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GENERAL  AND  DENTAL  PATHOLOGY 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 
Columbia  University  Libraries 


http://www.archive.org/details/generaldentalpatOOende 


GENERAL  AND  DENTAL 

PATHOLOGY 

With  Special  Reference  to  Etiology  and  Pathologic  Anatomy 
A  Treatise  for  Students  and  Practitioners 

BY 

JULIO  ENDELMAN,  M.S.,  D.D.S. 

Professor    of    Special    Dental    Pathology,     College    of    Dentistry,    University    of    Southern 
California;    Editor    of    the    Pacific    Dental   Gazette;    Member    of    the    Southern    Cali- 
fornia   Dental    Association,    the    California   State    Dental   Association,    and   the 
National    Dental    Association;    Corresponding    Member    of    the    Societe 
Odontologique    de    Fiance.    Honorary    Member    of    the    Sociedad 
Odontologica    de    Chile,    S.    A.,    etc. 

AND 

A.  F.  WAGNER,  A.M.,  M.D. 

Professor  of  General   Pathology,   College   of   Dentistry,   University   of   Southern   California; 
Pathologist  and  Autopsy   Surgeon  of  the  County  and   City  of  Los  Angeles;   Mem- 
ber  of   L,os   Angeles    County    Medical    Society,    California    State    Medical 
Association,     American     Medical     Association,     etc. 


WITH  440  ILLUSTRATIONS,  OF  WRICK  340  IN  THE  SECTION  ON 

DENTAL  PATHOLOGY  ARE  ORIGINAL,  AND 

FOUR  COLORED  PLATES 


ST.  LOUIS 

THE  C.  V.  MOSBY  CO. 

1920 


Copyright,  1920,  By  C.  V.  Mosby  Company 

(All   rights   reserved) 


Press  of 

C.   V.   Mosby  Company 

St.  Louis 


TO 

EDWARD  C.  KIRK,  D.D.S.,  Sc.D.,  LL.D. 

Scientist,  Teacher,  Author 

From  Whom  the  Authors  Eeceived  the  Instruction  in 
Dental  Pathology  Which  Constitutes  the  Foundation 
op  the  Section  of  This  Book  Devoted  to  That  Purpose, 
and  in  Appreciation  of  His  Contributions  to  Dental 
Science,  This  Book  is  Gratefully  Dedicated. 


P  RE  FACE 

It  has  been  the  aim  of  the  authors  to  treat  the  subject  from  the 
standpoint  of  gross  and  microscopic  pathology,  realizing  that   the 
needs  of  the  dental  student  call  for  just  that  character  of  infor- 
mation.    It  is,  of  course,  assumed  that  the  object  in  undertaking 
the  study  of  pathology  is  to  the  effect  that  the  information  neces- 
sary to  treat  diseases  upon  a  rational  basis  may  be  available;  there- 
fore the  clinical  aspects  of  the  maladies  discussed  throughout  the 
text  have  been  worked  out  on  the  basis  of  the  structural  changes  in- 
duced in  the  tissues  by  various  forms  of  irritation.     The  clinic  and 
the  laboratory  have  been  made  use  of  extensively  in  the  collection 
of  the  data  and  in  their  arrangement  in  sequential  order,  and  an 
effort  has  been  made  to  include  only  tangible  information,  excluding 
all  statements  of  more  or  less  speculative  character.     The  book,  it 
is  hoped,  will  be  a  help  to  dental  students  by  imparting  a  founda- 
tional knowledge  of  the  subject  and  by  rendering  less  complicated 
the  interpretation  of  pathologic  phenomena  in  the  field  of  dental 
diagnosis.     The  comprehension  of  dental  pathology  rests  upon  a 
clear  conception  of  those  abnormal  phenomena  which,  because  they 
may  develop  in  any  organ  or  tissue  of  the  body,  are  grouped  under 
the  heading  of  general  pathology.     Practically  all  the  illustrations 
in  the  section  on  Dental  Pathology  are  original,  and  this  feature  of 
the  book,  we  trust,  will  greatly  assist  the  student  in  his  analysis  of 
the  pathologic  anatomy  of  the  diseases  with  which  he  concerns 
himself. 

We  are  greatly  indebted  to  Dr.  Lewis  E.  Ford  for  placing  at  our 
disposal  the  laboratories  and  clinical  material  of  the  College  of 
Dentistry  of  the  University  of  Southern  California  and  for  his 
friendly  encouragement  and  help.  To  Dr.  A.  C.  LaTouche  we  are 
indebted  for  many  courtesies  extended  to  us  during  the  prepara- 
tion of  the  manuscript  and  illustrations  and  for  the  use  of  the 
microscopical  sections  from  which  Figs.  292,  293,  and  -105  were 
made,  and  for  the  original  photograph  of  Fig.  401. 

To  Dr.  Carroll  W.  Jones,  who  greatly  aided  us  in  the  preparation 
of  the  manuscript  for  the  press  and  in  the  revision  of  the  proofs, 
we  gratefully  acknowledge  our  appreciation.     To  Dr.  James  D. 


PREFACE 

McCoy  the  authors'  thanks  are  due  for  repeated  courtesies  and  sug- 
gestions and  for  his  cooperation  in  gathering  the  data  for  the  chap- 
ter on  systemic  infections ;  all  the  radiographs  in  that  chapter  were 
supplied  by  Dr.  McCoy,  without  whose  assistance  its  preparation 
would  have  been  greatly  handicapped.  To  Dr.  E.  F.  Tholen  we  ex- 
press our  thanks  for  the  originals  of  Figs.  346,  347,  348,  and  349, 
and  to  Dr.  C.  F.  Oakman  for  the  use  of  Fig.  342.  Our  thanks  are 
also  due  to  Professor  Win.  J.  Gies,  of  Columbia  University,  for  hav- 
ing placed  at  our  disposal  the  literature  covering  his  valuable  inves- 
tigation in  the  domain  of  dental  science ;  from  this  we  have  quoted 
freely,  especially  in  the  chapter  on  dental  caries.  "We  are  also  in- 
debted to  Dr.  H.  P.  Pickerill  for  the  use  of  Figs.  93,  94,  and  95 
from  his  excellent  work  ' '  The  Prevention  of  Dental  Caries  and  Oral 
Sepsis. ' '  Our  thanks  for  the  loan  of  cuts  are  due  to  the  publishers 
of  the  following  works:  Stengel  and  Fox's  "Pathology,"  Bailey's 
"Textbook  of  Normal  Histology,"  Delafield  and  Prudden's  "Text- 
book of  Pathology,"  McFarland's  "Pathology,"  McConnell's 
"Pathology  and  Bacteriology  for  Dentists,"  Black's  "Operative 
Dentistry,"  Ziegler's  "Textbook  of  General  Pathology,."  Blair's 
"Surgery  and  Diseases  of  the  Mouth  and  Jaws,"  "American  Text- 
book of  Dentistry, ' '  The  Dental  Cosmos,  The  Dental  Summary,  and 
others.  The  courtesy  extended  by  Dr.  F.  W.  Frahm  in  offering  sug- 
gestions which  are  incorporated  in  the  chapter  on  macroscopic 
deformities  is  also  acknowledged.  The  authors  desire  to  thank 
Dr.  W.  A.  Danielson  of  the  Chicago  College  of  Dental  Surgery, 
for  valuable  suggestions  in  the  text. 

To  Dr.  Gordon  B.  New  of  the  Mayo  Clinic,  for  contributing  the 
chapter  on  Cystic  Odontomas,  and  to  Dr.  J.  Walter  Reeves,  for 
contributing  the  chapter  on  Malformations,  the  authors  acknowl- 
edge their  obligation. 

The  authors  wish  to  extend  their  thanks  to  the  publishers  for 
their  hearty  cooperation. 

Julio  Endelman 
A.  F.  Wagner 

Los  Angeles,  Cal. 


CONTENTS 

PART  I 
GENERAL  PATHOLOGY 

CHAPTER  I 


PAGE 
21 


Introductory      

Pathology,  21;  Disease,  21;  The  Cell,  23;  Anatomy  of  the  Cell,  24; 
The  Chemistry  of  the  Cell,  26;  The  Physics  of  the  Cell,  29;  Stain- 
ing Reactions  of  the  Cell,  30;  The  Physiology  of  the  Cell,  32;  Ori- 
gin of  the  Blastodermic  Layers,   34. 

CHAPTER  II 

The  Etiology  of  Diseases 37 

Etiology  of  Disease,  37;  Age,  28;  Sex,  28;  Race,  29;  Idiosyncrasy, 
39;  Traumatisms,  39;  Injurious  Occupations,  39;  Unsanitary  Sur- 
roundings, 40;  Habits,  40;  Heredity,  4;  Specific  or  Determining 
Causes,  41;  Traumatism,  41;  Heat,  41;  Cold,  42;  Atmospheric  Pres- 
sure, 43;  Electricity,  43;  Light,  43;  X-rays,  44;  Chemical  Agents, 
44;   Living  Organisms,  44;   Autointoxication,  44. 

CHAPTER  III 

4.p; 

Pathologic    Processes        

Retrograde  Processes,  45;  Atrophy,  45;  Degenerations  (or  Meta- 
morphoses), 47;  Cloudy  Swelling,  Parenchymatous  or  Granular  De- 
generation, 48;  Fatty  Degeneration,  48;  Mucoid  Degeneration,  50; 
Colloid  Degeneration,  52;  Hyaline  Degeneration,  54;  Amyloid  De- 
generation (Waxy,  Baeony,  or  Lardaceous  Degeneration),  56;  In- 
filtrations, 59;  Fatty  Infiltration,  59;  Pigmentary  Infiltration,  61; 
Calcareous  Infiltration,  67;  Concretions  of  Concrements,  69;  Hy- 
dropic, Dropsical,  or  Serous  Infiltration,  70;  Glycogenic  or  Glycog- 
enous  Infiltration,  71;  Necrosis,  72;  Coagulation  Neorosis,  73; 
Liquefaction  Necrosis,  75;  Cheesy  Necrosis,  or  Caseation,  76;  Fat 
Necrosis,  77;  Focal  Necrosis,  78;  Gangrene,  79. 

CHAPTER  IV 

The  Circulatory  Changes 8j 

Ischemia,  or  Local  Anemia,  82;   Hyperemia,  83;   Active  Hyperemia, 


Z  CONTEK 

[yperemia,  -  tatic  <       _  ,  85;  Hemorrl    . 

35;  ,  87;    Throml    sis,  87  fcs,  92; 

Edema,  Dropsy  or  Anasarca. 

CHAPTEB  V 

Inflammation"  

Etio    _         -  Pal        gy  of  A     I     [nflammation,  98;   Edema- 

tons  or  Serous,  100;  Fibrinous,  100;  Diphtheritic  or  Cron] 

'ormation,  1<i2;  Phlegmonous  Inflamma- 
tion,  103;  Catarrhal  Inflammation,  104;   Parenchymatous  Inflamma- 
tion,  10.j;    Interstitial   Inflammation.    ]'>>'<:    Hemorrhagic    Inflamma- 
tion,   106;    Neerotie   or   G      _  is   Inflammation,   106;    Prod;, 
Inflammation.    106;    Beg  108;    Pathologic    Anal 
Patli' >logic   Regeneration,  108;    Metaplasia,   11":   Heteroplasia,  110. 

CHAPTEB  VI 

KESsrvx  Tissue  Changes Ill 

Hypertrophy,    111;    Etiology,    111;    G  .   .    112;    Micro- 

pic  Pathology,  112;  Pathologic  Physiology,  112:  L12. 

CHAPTEB  VII 

Tumors       113 

Theories  of  Origin  and  Causation,  113;  Fibromata,  117:  Myxomata, 
119:    Chondromata,   12";   Chordomata,   121;    Osteomata,  121;   Odon- 
tomata,    122;    Lipomata,    122:    Sarcomata.    123;    Bound-celled    - 
comata,  121;  Spindle-cel        3       imata,  127:  Melanotic  Sarcoma,  or 
Melanomata,  127;  Giant-celled  8arc  ,128;  Bhabdomyomata,  130 ; 

Leiomyomata,  130;  Glioma.  i:;2:  Glioma  Ganglionare,  or  Ganglionic 
Glioma,  or  Neuroma,  133;  Angiomata,  133;  Papillomata,  135; 
Adenomata,  138;  Carcinomata,  139;  Epithelioma,  141;  Adenocarcin- 
omata,  143;  Scirrhous  Carcinoma,  14:: ;  Medullary  Carcinoma,  14-",; 
Endotheliomata,  146;  Teratomata,  148;  Dermoid  I  sts.  18;  Hyper- 
nephroma,   L48      '     •-.   14f». 

CHAPTEB  VIII 

The  Pathology  of  Infectious  Diseases 152 

The  Pathology  of  Infectious  Diseases,  152;  Suppurative  Diseases, 
154;  Epidemic  '  spinal  Meningitis,  156;  Gonorrhea,  157;    - 

Chancre,  or  Chancroid,  158;   Pneumonia,  or  Pneumonitis,  1~>9;  Bron- 
chopneumonia or  Lobular  Pneumonia,   161;   Tuberculosis,  K>4:   Lep- 
7      -    philis,  or  Lues  (or  '-Gnat  Pox"),  168;   Glanders,  or 
E'juinia,   171;    The   Toxemic   Diseases,   172;    Tetanus   or  Lock   Jaw, 


CONTENTS  5 

PAGE 

L72;  Diphtheria,  17:'.;  Asiatic  Cholera,  L73;  Typhoid  Fever,  171; 
Bacillarv  Dysentery,  17");  Malta  Fever  or  Mediterranean  Fever,  17'i; 
Anthrax,  176;  Malignanl  Edema,  177;  Gas s  Edema,  177;  Bu- 
bonic Plague,  L76;  [nfluenza,  178;  Epidemic  Conjunctivitis,  17!); 
Whooping  Cough  or  Pertussis,  17!»;  Vincent's  Angina,  179;  Relaps- 
ing Fever,  179;  The  Higher  Bacteria,  180;  (Trichomycetes,  Chalam 
ydobacteriacese) ,  180;   Leptothrix  Infections   (Leptotrichoses),   180; 

Cladothrix  and  Nocardia   [nfections  or  Mycoses,  180;   Actin ycosis, 

181;  Mycetoma,  or  Madura  Foot  of  India,  182;  Blastomycosis  or 
Saccharomyeosis,  1 SU ;  Oidiomycosis,  183;  Mycoses  due  to  Molds,  or 
Hyphomycetes,  183;  The  Protozoan  Infect  ions,  IS.");  Amebic  Dysen- 
tery, 185;  Trypanosomiasis,  186' ;  Leishmaniases,  1 S7 ;  Malaria, 
187;  Coccidiosis,  190;  Infectious  Diseases  Caused  by  Undetermined 
Microorganisms,  190;  Measles,  190;  German  Measles,  1!»1  ;  Chicken 
Pox  or  Varicella,  191;  Scarlet  Fever  or  Scarlatine,  191;  Mumps,  or 
Acute  Epidemic  Parotitis,  191;  Acute  Poliomyelitis,  or  Infantile 
Paralysis,  1!>2;  Acute  Articular  Rheumatism,  1D2;  Dengue,  193; 
Yellow  Fever,  or  Typhus  Ieteroides,  193;  Typhus  Fever,  194;  Small- 
pox, or  Variola,  L94;  Foot-and-mouth  Disease,  194;  Rocky  Mountain 
Fever,   195;   Metazoa,  195;  The  Cestodes,  or  Tapeworms,  198. 

CHAPTER  IX 

M  W. FORMATIONS  208 

Malformations  by  Excess,  208;  Malformations  by  Defect,  209;  Hare- 
lip and  Cleft  Palate,  211. 


PART  II 
DENTAL  PATHOLOGY 

CHAPTER  X 

Introduction 213 

Predisposing  and  Exciting  Causes,  213;  Lowered  Vital  Resistance, 
214;  Exciting  Causes,  21-1;  Predisposing  Causes  of  Dental  Disease, 
215. 

CHAPTER  XI 

Enamel,  Dentin,  and  Cementttm 217 

Normal  Histologic  Considerations,  217;  Normal  Enamel,  217;  Dentin, 
228;    Cementum,   233. 


4  CONTEXTS 

CHAPTEE  XII 

PAGE 

Development  of  the  Teeth 241 

Dentin,  246;  Cementum  and  Peridental  Membrane,  248. 

CHAPTEE  XIII 

Hypoplasia,  Microscopic  axd  Macroscopic 250 

Dental  Hypoplasia,  251;  Enamel,  Dentin,  and  Cementum,  251. 

CHAPTEE  XIV 

Macroscopic  Deformities  of  the  Teeth 264 

Abnormalities  of  Form  Affecting  the  Crowns  and  Boots  of  the  Per- 
manent Teeth,  264;  Geminated  Teeth,  284. 

CHAPTEE  XV 

Abnormalities  ix  the  Number  of  Teeth 287 

Supernumerary  Teeth,  287. 

CHAPTEE  XVI 

Abnormalities  ix  the  Number  of  Teeth 291 

Absence  of  Teeth,  291. 

CHAPTEE  XVII 

Hutchixsox's  Teeth  axd  Other  Syphilitic  Stigmata 299 

Hutchinson's  Teeth  and  Other  Syphilitic   Stigmata,  299. 

CHAPTEE  XVIII 

Dental   Caries       306 

Historical  Data,  306. 

CHAPTEE  XIX 

Dental  Caries  (Coxt'd  ) 311 

General  Considerations,  311;  Predisposing  Causes,  317. 

CHAPTEE  XX 

Pathologic  Processes  ix  Dextal  Caries 322 

Pathologic  Processes  in  Dental  Caries,  322. 

CHAPTEE  XXI 

Caries   of  the   Examel 331 

Etiology  and  Pathologic  Anatomy,  331. 


CONTENTS  0 

CHAPTER  XXI] 

PAGE 

Gabies  of  Dentin  and  Oementxjm 340 

Etiology  and  Pathologic  Anatomy,  340 j  Transparent  Zone  or  Zone  of 
Tomes,  344;  Pigmentation,  .".17;  The  Decay  of  Cementum,  349. 

CHAPTER  XXIII 

Rtpercementosis 350 

General  Considerations,  350;  Etiology  and  Pathologie  Anatomy,  352. 

CHAPTER  XXIV 

Abrasion   and  Erosion       356 

Etiology  of  Abrasion,  356;  Pathologic  Anatomy  of  Abrasion,  357; 
Etiology  of  Erosion,  359;   Pathologic  Anatomy  of  Erosion,  365. 

CHAPTER  XXV 

The  Saliva 366 

Normal  and  Pathologic  Considerations,  366;  Color,  367;  Odor,  368; 
Taste,  368;  Constituents  of  the  Saliva,  369;  Mucin,  369;  Ptyalin, 
370;  Albumin,  371;  The  Sulphocyanates,  371;  Inorganic  Constit- 
uents, 372;  Reaction,  373. 

CHAPTER  XXVI 

The  Gums  and  Gingiva 375 

Normal  and  Pathologic  Considerations,  375;  Gingiva?,  376;  Normal 
and  Pathologic  Considerations,  376;  Functions,  378. 

CHAPTER  XXVII 

Calcareous  Deposits 381 

Etiology,  381;  Lesions  in  the  Investing  Tissues  Caused  by  Salivary 
Calculi,  387. 

CHAPTER  XXVIII 

Subgingival  Deposits 390 

Etiology,  390;  Lesions  Produced  by  Subgingival  Deposits:  Chronic 
Gingivitis,  392;  Pathologic  Anatomy,  392. 

CHAPTER  XXIX 

Diseases  of  the  Peridental  Membrane 402 

Horizontal  Fibers,  405;  Oblique  Fibers,  405;  Apical  Fibers,  406; 
Alveolar  Crest,  406;  Free  Gingiva,  406;  Transseptal  Fibers,  406. 


b  CONTEXTS 

CHAPTER  XXX 

PAGE 

Xonseptic  Pericementitis 408 

Nonseptic  Pericementitis,  408. 

CHAPTER  XXXI 

Septic  Pericemental  Inflammation  and  Acute  and  Chronic  Dento- 

alveolar  abscess 412 

Prophylaxis  of  Pulp  Involvements,  414 ;  Etiology  of  Septic  Apical 
Pericementitis,  415;  Periapical  Infection  by  the  Hematogenic  Route, 
421;  Recovery  from  Periapical  Infections,  Acute  and  Chronic  Proc- 
esses, 422. 

CHAPTER  XXXII 

Acute  Apical  Dentoalveolar  Abscess 424 

Etiology,  424;   Clinical  Symptoms,  425;   Sinus  Formation,  427. 

CHAPTER  XXXIII 

Pathologic  Anatomy  of  Acute  Dentoalveolar  Abscess 433 

Pathologic  Anatomy  of  Acute  Dentoalveolar  Abscess,  433. 

CHAPTER  XXXIV 

Chronic  Dentoalveolar  Abscess '436 

Etiology  and  Pathologic  Anatomy,  436;  Difference  in  the  Pathology 
of  Acute  and  Chronic  Dentoalveolar  Abscess,  443;  Bacteria  of  Septic 
Pericementitis  and  Dentoalveolar  Abscess,  4.12. 

CHAPTER  XXXV 

Bone 455 

Normal  and  Pathologic  Considerations,  455 ;  Bone  Involvement  in 
Dentoalveolar  Abscess,  457;  Xecrosis,  Caries,  and  Rarefying  Ostei- 
tis of  the  Alveoli  and  of  the  Jaws — Xecrosis  of  the  Apical  Areas  of 
Roots,  462. 

CHAPTER  XXXVI 

Periostitis  of  the  Jaw 467 

Periostitis  of  the  Jaw,  467. 

CHAPTER  XXXVII 

Pyorrhea  Alveolaris 471 

Historical  Sketch,  471;  General  Considerations,  473;  Pyorrhea  Al- 
veolaris Caused  by  Salivary  Calculi,  474;  Pyorrhea  Alveolaris  Caused 
by  Subgingival  Deposits,  476;  Pyorrhea  Alveolaris  of  Systemic  Ori- 
gin, 487. 


CONTENTS  I 

CHAPTEB   WW  III 

PAGE 

Pyorrhea  Alveolaris  and  Pericemental  Abscess  of  Gouty  Origin    .     195 
Etiology  and   Pathologic  Anatomy  of  Pyorrhea   Alveolaris  and   Peri 
cemental  Abscess  of  Gouty  Origin,   l'.»<j. 

CHAPTEB   XXXIX 

The  Dental  Pulp  and  Its  Diseases 500 

Histologic  Constituents,  500;  Fibers  of  Tomes,  505;  Diseases  of  the 
Pulp,  505;  General  Predisposing  Causes,  -106;  Local  Predisposing 
Causes,  507 ;  Exciting  Causes:  General,  508;  Exciting  Causes: 
Local,  509. 

CHAPTER  XL 

Calcific  Degenerations  of  the  Pulp  and  of  the  Dentinal  Tubuli     .     510 
Secondary  Dentin,  510;   Pulp  Nodules,  514. 

CHAPTER  XLI 

Pulp  Hyperemia 518 

General  Considerations,  518;   Etiology,  519. 

CHAPTER  XLII 

Gangrene  of  the  Pulp — Putrescent  Pulp 523 

General  Considerations,  523;  Pulpitis,  525;  Nonseptic  Pulpitis,  525; 
Septic  Pulpitis,  526;  Pathologic  Anatomy,  528;  Pulp  Hypertrophy, 
530. 

CHAPTER  XLIII 

Cystic  Odontomas.     (By  G.  B.  New,  M.B.,  Mayo  Clinic,  Rochester, 

Minn.) 532 

Simple  Cysts  of  Type  A,  532;  Simple  Cysts  of  Type  B,  534;  Adaman- 
tinomas, 535 ;  Pathologic  Anatomy,  539. 

CHAPTER  XLIV 

Mouth  Infections  in  Their  Relation  to  Systemic  Disease     ....     544 
Secondary  Focal  Infections,  5G2. 

CHAPTER  XLV 

Diseases  of  the  Gingivae,  Gums  and  Oral  Mucous  Membrane  .  .  .  565 
Simple  Stomatitis  (Stomatitis  Simplex),  565;  Catarrhal  Stomatitis, 
566;  Ulcerative  Stomatitis,  567;  Mercurial  Stomatitis,  569;  Aphthae 
— Canker  Sores — and  Aphthous  Stomatitis,  570;  Thrush,  571;  Herpes 
Labialis,  572;  Affections  of  the  Tongue,  572;  Fleers  of  the  Tongue, 
572;  Leucoplakia  of  the  Tongue,  573. 


ILLUSTRATIONS 

FIG.  PAGE 

1.  Diagram    of    a   typical    cell 24 

2.  Diagrams  of  successive  phases  of  mitosis 34 

2.  Diagrams  of  successive  phases  of  mitosis 35 

3.  Brown  atrophy  of  the  heart  muscle 46 

4.  Albuminous    degeneration — kidney        47 

5.  Fatty  degeneration — kidney 49 

6.  Mucoid  degeneration  of  fibrous  tissue 51 

7.  Colloid   degeneration    of    the   thyroid    gland 53 

8.  Hyaline  degeneration  of  an  ovarian  capillary 54 

9.  Amyloid  infiltration  of  capillary  walls  in  kidney  glomerulus     ....  56 

10.  Fatty  infiltration  of  the  liver 60 

11.  Anthracosis   of  the  lung 65 

12.  Calcareous  infiltration  of  the  wall  of  a  small  artery  from  the  wall  of 

a   gumma   of   the   liver 68 

13.  Dropsical  infiltration   of  the   epithelial  cells   of  a  carcinoma   of  the 

breast 71 

14.  Coagulation   necrosis    of    the    hepatic    cells    in    a    case    of    puerperal 

eclampsia 74 

15.  Large  tubercle  of  the  lung,  showing  cheesy  necrosis 77 

16.  Focal  necrosis  in  the  liver  in  pneumonia 78 

17.  Senile  dry  gangrene  of  the  lower  extremity,  showing  line  of  demar- 

cation         80 

18.  Chronic  passive  congestion  of  the  liver 84 

19.  Old  anemic  infarct  of   spleen 94 

20.  Acute    Inflammation        100 

21.  Inflammation    of    the    mesentery 100 

22.  Acute  inflammation 100 

23.  Pseudomembranous  inflammation  of  the  uvula 101 

24.  Tuberculous  ulceration  of  the  intestine 104 

25.  Acute    bronchial    catarrh 105 

2'?>.  Chronic   interstitial   nephritis 105 

27.  Loops  of  blood-vessels  in  granulation  tissue 107 

28.  Formation  of  new  blood-vessels  as  seen  in  the  tail  of  a  tadpole     .     .     .  107 

29.  Fibroblasts    forming    fibrous    tissue 108 

30.  Eegeneration   of   epithelium 109 

31.  Hard  fibroma 117 

32.  Soft  fibroma  of  the  subcutaneous  tissue 118 

33.  Section   of    a   myxosarcoma 119 

34.  Chondroma    of    the    thumb 120 

35.  Osteoma   of   the   lower   jaw 122 

8 


ILLUSTRATIONS 


PIG. 


PAGE 


Small   round-celled  sarcoma 125 

37.  Large  round  celled  sarcoma 126 

38.  Alveolar   sarcoma       * 126 

39.  Spindle-cell  sarcoma  of  the  mammary  gland 127 

40.  Large    spindle-celled    sarcoma 128 

II.  Melanosarcoma        1-:' 

42.  Giant   cell   sarcoma  of  the  thigh 129 

4:;.  Metastatic    melanosareoma    of   lung 130 

44.  Submucous  fibroid  in  the  uterus 131 

45.  Glioma    of    the    brain 132 

46.  Cavernous  angioma  of  liver ■  ....  134 

17.   Papillomata    of   the    vocal    cords 137 

-.   Papilloma    of    the    scalp 137 

49.  Adenoma  of  the  mammary  gland 138 

.   Squamous  epithelioma 142 

51.  Adenocarcinoma   of  the  body   of   the   uterus 1-4 4 

52.  Scirrhous  carcinoma  of  breast 145 

53.  Medullary  carcinoma  of  breast 146 

.">4.  Endothelioma  of  the  dura  mater 147 

55.   Finer  structure  of  the  adenomatous  form  of  hypernephroma     .     .     .  149 

50.  Chorionepithelioina    or    syncytioma    malignum 150 

57.  Cyst    of   the   parovarium I'1 

58.  Acute  urethritis 1**8 

59.  Acute'   lobar   pneumonia 160 

60.  Acute   lobar    pneumonia.     Later    stage 161 

61.  Bronchopneumonia.       Child 162 

02.  Miliary   tubercles   in  the   liver 165 

63.  Miliary  tubercle  of  the  human  form 165 

64.  Nodular  leprosy 1^8 

65.  Gummatous  meningo-encephalitis 170 

66.  Typhoid  fever,  showing  necrosis  of  Peyer's  patches  and  intense  con- 

gestion of  the  bowel 175 

67.  Actinomycosis    of    the    tongue 181 

68.  Blastomycosis I82 

69.  Invasion  of   a  human   hair   by   trichophyton 184 

70.  Trypanosoma  gambiense 186 

71.  The  common  liver-fluke  enlarged  to  show  the  anatomic  characters     .  197 

7  2.  Head  of  Taenia  solium 198 

7:'..  Taenia    echinoeoccus,    enlarged 200 

74.  Asearis   lumbricoides       201 

75.  Male  Trichocephalus  dispar  or  whipworm 202 

76.  Cephalic   extremity   of   uncinaria    duodenalis 203 

77.  Duodenum  showing  attached  uncinaria 203 

78.  Trichina   spiralis  with   its   connective-tissue   covering 205 

7!'.   Filaria    embryo,   alive   in  the   blood 206 


10  ILLUSTRATIONS 

FIG.  PAGE 

SO.  Female  acarus 207 

81.  Head  of  fetus  at  end  of  fifth  week 210 

82.  Head  of  fetus  in  the  seventh  week 210 

83.  Diagram   of  ordinary  harelip 211 

84.  Almost    complete    single    harelip 211 

85.  Diagram    of    median    harelip 211 

8G.  Cleft   of  the  hard   and   soft  palate 212 

87.  Complete  double  cleft  in  an  infant 212 

88.  Area  of  normal  dentin  and  enamel 218 

89.  Area  of  normal  dentin  and  enamel  from  ground  section  of  area  near 

apex  of  incisor  of  man 219 

90.  Contrast   between    normal    enamel    and   decalcified    enamel     ....  220 

91.  Dentoenamel    junction        221 

92.  Ground  section,  showing  junction  of  enamel  and  cementum     .     .     .  222 

93.  Imbrication  lines  on   lower  incisor  of  sclerotic  type 224 

94.  Imbrication  lines  on  lower  incisor  of  malaeotic  type 224 

95.  Calcarine  fissures  on  the  surface  of  a  malaeotic  molar 225 

90.  Decalcified  longitudinal  section  showing  butt  type  of  enamel-cemen- 

tum  junction 227 

97.  Longitudinal    section    of   upper   cuspid    showing   the   course    and    ar- 

rangement of  the   dentinal   tubuli    (Color  Plate)          228 

98.  A  field  of  dentinal  tubules 229 

99.  Transverse   section   of   dentin 229 

100.  Interglobular  spaces  of   Czcrmack   in  the   dentin 231 

101.  Longitudinal  ground  section  of  tooth   showing  fields  of  dentin  and 

enamel 232 

102.  Transverse  ground  section  at  the  apical  region  of  a  root     ....  2.",  1 

103.  Transverse  ground  section  of  tooth  at  the  beginning  of  apical  third 

of  root 235 

101.   Thick  area  of  cementum  in  the  bifurcation  of  the  roots  of  a  molar     .  23G 

105.  Longitudinal  ground  section  showing  hyaline  cementum,  etc.     .     .     .  237 

106.  Ground  section,  longitudinal,  showing  gingival  third  of  root     .     .     .  238 

107.  Ground   section,  longitudinal,   showing  hyaline  cementum   devoid   of 

lacunae   and   canaliculi       238 

108.  Longitudinal  ground  section  of  cementum,  showing  lacunae  in  areas 

near  dentin  and  fibers  of  pericemental  membrane  incased  in  the  ce- 
mentum           239 

109.  Longitudinal  ground  section  in  gingival  third 239 

110.  The  cementum   in   the  apical  region   of  the  roots   of   an   upper  first 

bicuspid        240 

111.  First   evidence   of  tooth   development 242 

112.  A  slightly  later  stage  than  in  the  preceding  illustration 243 

113.  The  four  sets  of  cells  of  the  enamel  organ 244 

114.  Same  stage  of  development  as  seen  in  the  preceding  illustration     .     .  247 


ILLUSTRATIONS  11 
FIfi.                                                                                                                                                                   PAGE 

115.  Calcification  of  the  deciduous  teeth 248 

116.  Calcification   of  the   permanent   teeth 248 

117.  Hypoplastic  defeets  of  the  enamel 251 

118.  Hypoplastic   defect    of  the  enamel 252 

119.  Hypoplasia  of  the  enamel  producing  an  external  macroscopic  defect 

on  the  labial  surface  of  an  incisor 255 

120.  Hypoplasia  of  the  enamel  in  the  approximal  surface  of  an  incisor     .  256 

121.  A  case  of  enamel  agenesia 257 

122.  Decalcified  section  showing  a  multitude  of  interglobular  spaces     .     .  257 

123.  Hypoplasia  of  the  enamel  in  the  shape  of  a  slight  reddish  brown 

discoloration 259 

124.  Hypoplasia  of  the  enamel  in  the  shape  of  intense  reddish  brown  dis- 

coloration        259 

125.  A  case  of  biown  stain  affecting  the  enamel  on  the  labial  surfaces  of 

the  central  and  lateral  incisors  only 259 

126.  A  slight  hypoplasia  of  the  enamel  on  the  labial  surface  of  an  upper 

cuspid 260 

127.  Hypoplasia  of  the  enamel  on  the  labial  surface  of  an  upper  cuspid  260 

128.  Hypoplasia  of  the  enamel  on  the  labial  surfaces  of  upper  left  and 

upper  right  lateral  incisors,  semilunar  in  shape 260 

129.  Hypoplasia  of  the  enamel  in  an  upper  left  central  incisor     ....  260 

130.  Hypoplasia  of  the  enamel  in  an  upper  right  lateral  incisor     ....  261 

131.  Hypoplasia  in  the  crown  of  a  lower  molar 261 

132.  Hypoplasia  of  the  crown  of  an  upper  molar 261 

133.  Hypoplasia  of  the  enamel  in  upper  molars 261 

134.  Hypoplasia  of  the  enamel  in  lower  molars 262 

135.  Hypoplasia  of  the  enamel  in  an  upper  cuspid 262 

136.  Hypoplasia  of  the  enamel  in  an  upper  central 262 

137.  Overdeveloped  cervico-lingual  ridge  in  upper  left  lateral  incisor     .  265 

138.  Hypoplasia  of  the  cervico-lingual  ridge  of  upper  incisors     ....  265 

139.  Fissured  cervico-lingual  ridge  in  lateral  incisor 265 

140.  Photomicrograph  of  a  central  incisor  with  an  over-developed  cervico- 

lingual  ridge  simulating  a  cusp 266 

141.  Severe  hypoplasia  of  upper  central  incisor 267 

142.  Severe  form  of  hypoplasia  in  upper  incisor 267 

143.  Severe  form  of  hypoplasia  in  upper  incisor  involving  the  crown  and 

the   root        267 

144.  Hypoplasia  of  the  root  of  an  upper  incisor 267 

145.  Ground  section  of  specimen  shown  in  Fig.  144 268 

146.  Hypoplasia  of  the  incisal  third  of  an  upper  incisor 269 

147.  Peg-shaped  upper  lateral  incisor 269 

148.  An  upper  right  lateral  incisor  mesial  view-  with  a  labial  defection  of 

its  root 269 

149.  A  prong-like  process  on  the  lingual  surface  of  the  lower  lateral  in- 

cisor      269 


12  ILLUSTRATIONS 

FIG.  PAGE 

150.  Lower  lateral  incisor  with  two  roots 270 

151.  Severe  hypoplasia  of  upper  cuspid 270 

152.  A  marked  case  of  enamel  and  dentin  hypoplasia 270 

153.  A  series  of  upper  cuspids  with  unusually  short  roots 271 

154.  A  series  of  upper  cuspids  with  abnormally  long  roots 271 

355.  Distal  deflection  of  an  upper  right  cuspid 272 

156.  A  marked  deflection  to  the  mesial  in  an  upper  right  cuspid     .     .     .  272 

157.  Lower  cuspids  with  two  roots 272 

158.  Eadiogram  of  a  lower  right  cuspid  with  two  roots 273 

159.  Supernumerary   root   in   lower   cuspid 273 

160.  Marked  hypoplasia  of  the  crown  of  a  lower  cuspid 273 

161.  Upper  first  bicuspid  with  three  roots 273 

162.  Upper  right  first  bicuspid  with  three  roots 273 

163.  An  upper  second  bicuspid  with  a  bifurcated  root 273 

164.  An  upper  first  bicuspid  with  marked  deflection  of  the  lingual  root     .  273 

165.  Bifurcation  of  the  roots  of  an  upper  second  bicuspid 274 

166.  An  upper  bicuspid  with  three  roots 274 

167.  An  upper  first  bicuspid  with  an  abnormally  long  root 274 

168.  A  hypoplastic  upper  bicuspid 274 

169.  Pronounced  deflection  of  the  root  of  an  upper  bicuspid 274 

170.  Upper  left  second  bicuspid;   disproportion  between  the  size  of  the 

crown  and  that  of  the  root 275 

171.  An  upper  second  bicuspid  with  a  disproportionately  small  root     .     .  275 

172.  A  lower  first  bicuspid  with  two  roots 275 

173.  Lower  second  bicuspid  with  two  roots 275 

174.  A  lower  first  bicuspid  with  a  marked  deflection  of  its  roots     ....  275 

175.  Distal  deflection  of  the  root  of  the  lower  right  first  bicuspid     .     .     .  275 

176.  Disproportion  between  the  size  of  the  crowns  and  roots  of  lower  sec- 

ond   bicuspids       276 

177.  Hooked  root   in  lower   bicuspid 276 

178.  Disproportion  between  the  crown  and  root  of  a  lower  right  second 

bicuspid        276 

179.  Disproportion  between  the  size  of  the  crown  and  that  of  the  root  and 

deflections  of  the  root  of  lower  first  bicuspids         276 

180.  Hypoplasia  of  the  lingual  cusp  of  a  lower  first  bicuspid     ....  277 

181.  A   hypoplastic  lower  second  bicuspid 277 

182.  Lower  left  second  bicuspid  with  six  cusps 277 

183.  The  roots  of  an  upper  molar  united  by  bands  of  cementum     .     .     .  278 

184.  An  upper  second  molar  with  its  three  roots  fused  together  by  means 

of  cementum          278 

185.  Upper  left  third  molar  with   badly  deflected,   fused,   and  hyperce- 

mentosed  roots      278 

186.  An  upper  first  molar  with  hooked  roots 278 

187.  Deflection  to  buccal  and  distal  roots  of  upper  first  molar     ....  279 

188.  A  supernumerary  root  in  upper  molar 279 


ILLUSTRATIONS  13 
FIG.                                                                                                                                                          PAGE 

L89.   Lower    right    first    molar   with   superrfumerary    root   on    the   lingual 

aspect • 280 

190.  Supernumerary  root  on  distobuccal  aspect  of  a  lower  first  molar     .     .  280 

191.  A  lower  first  molar  with  a  supernumerary  root  between  the  mesial 

and  distal  roots  on  the  lingual  aspect 280 

192.  A  lower  firsl   molar  with  three  roots 280 

L93.   A  lower  first  molar  with  three  roots;  supernumerary  root  on  incisal 

aspect 280 

194.  Four    well-developed   roots   iu    lower   left    second   molar          ....  281 

195.  A  hypoplastic  lower  third  molar 281 

196.  Dwarfed    upper    third    molar 282 

197.  Dwarfed   lower   third    molars 282 

198.  Dwarfed    upper    third    molar 282 

199.  Hypoplastic  upper  third  molars 283 

200.  Marked  deviation  of  the  roots  of  an  upper  third  molar     ....  283 

201.  Upper  third  molars  with  double  deflection  of  the  buccal  roots  and 

single  deflection  of  the  lingual  roots 283 

202.  Geminated  deciduous  incisors 285 

203.  Geminated  upper  central  and  lateral  incisors 285 

204.  Geminated   molar   and  bicuspid;    possibly   two   bicuspids     ....  285 

205.  Geminated  upper  second  and  third  molars 285 

206.  Geminated  upper  second  and  third  molars 286 

207.  Geminated  upper  second  and  third  molars 286 

208.  Enamel  pearl  on  upper  left  second  molar  located  in  the  concavity  on 

the  lingual  root  which  shows  a  tendency  toward  bifurcation     .     .  286 

209.  Enamel  pearl  in  upper  right  first  molar 286 

210.  A  peg-shaped  supernumerary  tooth  between  the  upper  central  incisors  287 

211.  Two  tuberculated  supernumerary  incisors  in  the  same  arch     .     .     .  287 

212.  A  tuberculated  supernumerary  tooth  between  the  incisors     ....  288 

213.  A  peg-shaped  supernumerary  tooth  located  lingually  to  the  upper  in- 

cisors          288 

214.  A   supernumerary  central  in  perfect   alignment   between  normal  in- 

cisors           288 

2\~>.  A  supernumerary  upper  incisor  fused  to  the  normal  central  incisor  289 

216.  Supernumerary  molar  between  the  upper  second  and  third  molars     .  289 

217.  A    fourth    molar    in   place 289 

218.  Deciduous  upper  second  molar  retained  until  late  in  life     ....  292 

219.  A  retained  lower  left  second  deciduous  molar 292 

220.  Absence  of  the  upper  right  lateral  incisor 293 

221.  Xoneruption   of   permanent   lower   first   molar 293 

222.  Xoneruption   of  permanent   cuspid 294 

223.  Xoneruption    of   permanent    cuspid 294 

224.  Impaction  of  lower  third  molar 295 

225.  Impaction    of   third   molar 295 


14  ILLUSTRATIONS 

FIG.  PAGE 

226.  Impaction   of  lower  third   molar 296 

227.  Impaction  of  second  bicuspid   and   second   molar 296 

228.  Impacted    lower    third    molar 297 

229.  Hutchinson's  teeth.     Sulciform  erosions  of  incisors 300 

230.  Hutchinson  teeth.     Cuspal  erosions  of  canines  and  molars     ....  300 

231.  Hutchinson's  teeth.     Cuspal  atrophy  of  canines  and  first  molars     .     .  301 

232.  Multiple  sulciform  erosions,  general,  and  involving  the  bicuspids     .  301 

233.  Lingual  aspects  of  preceding  illustrations.     Hutchinson's  teeth     .     .  301 

234.  Hutchinson   teeth.     Honeycomb   erosions 302 

235.  Hutchinson    teeth.      Mierodontism 303 

236.  Complete  congenital  absence  of  teeth  in  the  upper  arch 303 

237.  Defective    fissure    in    a    molar 318 

238.  Typical  conical  form  of  penetration  of  caries  into  the  dentin     .     .     .  326 

239.  Microorganisms  in  the  structure  of  the  dentin 327 

240.  Microorganisms  in  the  structure  of  the  dentin 327 

241.  Microorganisms  in  the  structure  of  the  dentin 329 

242.  Microorganisms  in  the  structure  of  the  dentin 329 

243.  Artificial  decalcification  of  the  enamel  by  one  per  cent  hydrochloric 

acid    simulating    caries 332 

244.  Caries  of  enamel  at  the  deepest  portion  of  the  cavity 333 

245.  Caries  of  enamel  in  proximal  surfaces 335 

246.  Caries  of  enamel  in  a  proximal  surface  in  which  caries  lias  made  con- 

siderable  progress 336 

247.  Caries  of  enamel    in   a    pit 337 

248.  Progress  of  enamel  caries  in  a  molar 338 

249.  Progress  of  enamel  caries  in  a  molar 339 

250.  Caries  of  dentin  showing  decalcification  of  the  organic  constituents 

and  conversion  into  a  soft  cartilaginous  mass 340 

251.  Caries   of   dentin   showing    decalcification    of   the   inorganic    constit- 

uents and  conversion  into  a  soft  cartilaginous  mass 341 

252.  Undermining  caries;   destruction  of  tooth  substance  from  within     .  342 

253.  Undermining  caries;    destruction  of  tooth  substance  from  within     .  343 

254.  Undermining  caries  of  approximal  surface;   undeeayed  enamel  cusp 

about  to  break  away 344 

255.  Caries    of    dentin 345 

256.  Transparent  zone  of  Tomes  in  dentin 346 

257.  Caries  of  enamel  and    dentin 348 

258.  Caries  of  eementum  on  labial  surface  of  abraded  upper  left  central 

incisor 348 

259.  Hypercementosis  of  lower  first  bicuspid  and  deflection  of  its  root     .  350 

260.  Hypercementosis  in  upper  rigid  second  molar 350 

261.  Hypercementosis  in  upper  bicuspid 351 

L'62.  Hypercementosis  of  root  of  lower  molar,  the  two  roots  are  united  by 

a  band  of  eementum 351 

263.  Hypercementosis  involving  the  three  roots  of  an  upper  molar     .     .     .  351 


ILLUSTRATIONS  1  5 

FIG.  PAGE 

264.  Hypercementosis  involving  the  apical  area  of  the  three  roots  of  an 

upper  molar • 351 

265.  Excessive  hypercementosis  in  :i  lower  molar        351 

2<><i.   Excessive   hypercementosis   in   ;i    molar   which    rendered    its   removal 

difficult    and   entailed   the   fracture   of   the   surrounding   alveolar 

process 351 

2t>7.   Hypercementosis  involving  the  three  roots  of  an  upper  left  first  molar  .''>-">2 

268.  Hypercementosis  of  the  posterior  rool  of  the  lower  first   molar     .     .  352 

269.  Nodular    form   of   hypercementosis 352 

270.  1?  sorption  of  dentin  and  obliteration  of  the  resorbed   area  by  ce- 

mentum 353 

271.  Hypercementosis  accompanied  by  dentin  resorption  and  filling  in  of 

the  resorbed  area  of  dentin  by  cementum 354 

272.  Abrasion— mechanical  wearing  away  of  the  cusps  of  a  lower  molar  :!-">7 

273.  A   series  of  incisors  which  have  suffered  from  slight  abrasion     .     .  358 

274.  Abrasion  of  the  incisal  edges  of  two  upper  central  incisors;  brown- 

ish discoloration  of  exposed  dentin 358 

275.  Photomicrograph  of  ground  section   of  one  of  the  abraded  teeth     .  359 
27<>.   Upper    right    cuspid 360 

277.  Upper  cuspids  which  for  many  years  have  been  the  seat  of  abrasion  360 

278.  Abrasion  of  lower  third  molar.     Complete  wasting  away  of  the  crown  361 

279.  Abrasion  of  lower  third  molar.     Complete  wasting  away  of  the  crown  361 

280.  Spiral-shaped   abrasion   in   upper  left   cuspid  caused   by   an    ill-fitting 

clasp 361 

£81.   A   series   of   abraded   lower   cuspids 361 

282.  Abrasion   of  upper   right  central  incisor 362 

283.  Abrasion  of  lingual  surface  of  upper  left  cuspid 362 

2S4.  Abrasion  of  the  labial  surface  of  the  lower  right  first  bicuspid     .     .  ."!fi2 

285.  Cup-shaped    abrasion   in   lower  molars 362 

286.  Cup-shaped  abrasion  in  lower  first  molar 363 

287.  Cup-shaped  abrasion  in  a  lower  molar 363 

288.  Cup-shaped    abrasion    in    lower    molar 363 

289.  Abrasion    in    a.   deciduous   molar 363 

290.  Action  of  acid  calcium  phosphate  in  conjunction  with  friction     .     .     .  364 

291.  Tubular  calcification  in   the  dentin 364 

292.  Normal    gingiva    of    sheep 376 

293.  Gingiva?    of    sheep 377 

294.  Human  gingiva 378 

295.  Salivary  calculi  on  the  lingual  surfaces  of  the  roots  of  lower  cuspids  383 

296.  Voluminous    salivary    calculus    with    shelf -like    formation      ....  384 

297.  Salivary   calculus  with   shelf-like   formation 384 

298.  Salivary   calculus   in   lower   right   incisor 384 

299.  Salivary  calculus  which  had  attained  considerable  size  and  had  caused 

exfoliation  of  the  tooth 384 


16  ILLUSTRATIONS 

FIG.  PAGE 

300.  Salivary  calculus  in  lower  incisor  which  had  caused  the  exfoliation 

of  the  tooth 385 

301.  Salivary  calculus  covering  all  of  the  crown  and  most  of  the  root  of 

the  tooth 383 

302.  Salivary  calculus  which  covered  a  large  area  of  crown  surface  and  all 

of   one-half  the  root   surface 385 

303.  Salivary  calculus  on  lower  right  cuspid  involving  approximately  two- 

thirds  of  the  root 385 

304.  Salivary  calculus  on  lingual  aspect   of  the  root  of  a  lower  central 

incisor 385 

305.  Salivary   calculus   covering  portion   of   the   labial   surface   of   lower 

right    central    incisor         385 

306.  Salivary  calculus  entirely  covering  the  buccal  surface  of  the  crown 

and  half  the  length  of  the  roots  of  an  upper  left  first  molar     .     .     386 

307.  Voluminous  salivary  deposits  upon  buccal  and  part  of  the  occlusal 

surfaces  of  an  upper  molar 386 

308.  Large  masses  of  salivary  calculi  removed  from  the  teeth  to  which 

they    were    attached 387 

309.  Large  masses  of  salivary  calculi 387 

310.  An  upper  lateral  incisor  with  its  root  covered  with  subgingival  de- 

posits          390 

311.  Subgingival  deposits  in  upper  right  lateral  incisor 390 

312.  Subgingival  deposits  in  upper  right  cuspid 390 

313.  Subgingival   deposits  in  upper   right   second  molar 391 

314.  Subgingival   deposits  in  upper   right   second  molar 391 

315.  Eoots  of  a  molar  covered  with  subgingival  deposits 391 

316.  Subgingival  deposits  on  the  anterior  and  posterior  roots  of  a  lower 

molar        391 

317.  Section  of  human  gingiva 393 

318.  Chronic    inflammation    of    gingiva 394 

319.  Chronic  inflammation  of  the  free  gingiva 395 

320.  Gingivitis,    chronic,    advanced    stage,    infection    progressing    toward 

peridental  membrane 396 

321.  Gingivitis,  chronic,  advanced  stage,  induced  by  subgingival  deposits  397 

322.  Progressive  chronic  gingivitis 398 

323.  Chronic    inflammation    of    gingiva 399 

324.  Chronic  inflammation  in  the  gingiva  which  has  spread  to  the  periden- 

tal   membrane 400 

325.  Progressive  chronic  gingivitis 401 

326.  Normal  peridental  membrane 403 

327.  Normal  peridental  membrane  in  situ 404 

328.  Normal  peridental  membrane  and  its  relation  to  cementum  and  al- 

veolar process       405 

329.  Chronic  dentoalveolar  abscess  of  an  upper  lateral  incisor  with  a  large 

area   of  rarefaction 416 


[LLUSTRATIONS  17 
FIG.                                                                                                                                                                      PAGE 

330.  Chronic  dentoalveolar  abseesa 416 

331.  Chronic  dentoalveolar  abscess  in  upper  firsl  and  second  left  bicuspids  416 

332.  Three  chronic  dentoalveolar  abscesses 416 

333.  Chronic  dentoalveolar  abscess 117 

334.  Chronic   dentoalveolar   abscesses 417 

335.  Chronii'  dentoalveolar  abscess 418 

336.  Chronic  dentoalveolar  abscess , 418 

337.  Chronic  dentoalveolar  abscess   (so-caUed  dental  granuloma)     .     .     .  419 
538.  Chronic  dentoalveolar  abscess  in  the  bifurcation  of  the  roots  (if  the 

lower    right    first    molar 420 

339.  Chronic  dentoalveolar  abscess  caused  by  the  perforation  of  the  disto- 

lingual  aspect  of  an  upper  second  bicuspid 420 

340.  Chronic  dentoalveolor  abscess  caused  by  a   fragment   of   a   broach 

broken  in  the  root  canal 420 

341.  Intraalveolar  root  fracture  of  an  upper  right  cuspid 420 

342.  Result  of  poulticing  the  face  in  connection  with  acute  dentoalveolar 

abscesses 428 

343.  Submental  fistula 430 

344.  A  chronic  dentoalveolar  abscess  (dental  granuloma) 437 

345.  Chronic  dentoalveolar  abscess 437 

346.  Dentigerous    or    root    cyst 442 

347.  Dentigerous  or  root  cyst 442 

348.  Dentigerous  or  root  cyst 442 

349.  Dentigerous  or  root  cyst 442 

350.  Chronic  dentoalveolar  abscess   (so-called  dental  granuloma)      .     .     .  444 

351.  Section  of  a  chronic  dentoalveolar  abscess 445 

352.  Chronic  dentoalveolar  abscess 446 

353.  Chronic  dentoalveolar  abscess 447 

354.  Chronic  dentoalveolar  abscess 448 

355.  Chronic  dentoalveolar  abscess 449 

356.  High  power  reproduction  of  cellular  elements  in  the  round-cell  infil- 

tration in   a   chronic  dentoalveolar   abscess 450 

357.  Alveolar  bone  in  the  periapical  region 458 

358.  Transverse    section    of    tooth 459 

359.  Arrangement  of  cancellated  bone  in  region  of  central  incisors     .     .  460 

360.  Bone  of  alveolar  process  and  two  cancellated  spaces 460 

361.  Arrangement    of   bono    in    incisal    region 461 

362.  Arrangement  of  bone  in  bicuspid  region 461 

363.  Arrangement  of  bone  in  molar  region 461 

326.  Beginning  resorption  of  the  apical  third  of  a  root  of  an  upper  central  465 

365.  Resorption  of  the  roots  of  a  lower  right  first  molar 465 

366.  Beginning  resorption  of  the  apical  third  of  a  root  of  an  upper  central     465 

367.  A  chronic  alveolar  abscess 465 

368.  Chronic  dentoalveolar  abscess 466 


18  ILLUSTRATIONS 

FIG.  PAGE 

369.  Sequestrum  that  came  away  attached  to  a  tooth  following  a  chronic 

dentoalveolar  abscess  of  long  standing 468 

370.  Subgingival  deposits  on  the  root  surfaces 475 

371.  Absence   of  approximal   contact  accounting  for  the   formation  of  a 

pocket  between  lateral  incisor  and  cuspid 47.1 

372.  Absence  of  contact  and  pyorrhea  pocket   formation 475 

373.  Absence  of  contact  and  pyorrhea  pocket   formation 475 

.",74.  Absence  of  contact  and  pyorrhea  pocket  formation 475 

375.  Absence  of  contact  and  pyorrhea  pocket   formation 475 

376.  An  area  of  gingivae  from  a   pyorrhea  pocket,  the  seat  of  a  chronic 

inflammation 476 

377.  Gum  tissue   overlying  a   pyorrhea   pocket   decalcified   section     .     .     .     477 

378.  Chronic  gingivitis  which  by  process  of  continuity  will  spread  to  the 

gums   and  peridental   membrane 478 

379.  Decalcified  transverse  section  of  upper  incisor 479 

3S0.  An   area   of  peridental  membrane  the  seat   of  chronic   inflammation 

in    pyorrhea    alveolaris 480 

381.  Chronic    inflammation    of    peridental    membrane 481 

382.  Transverse  section  showing  dentin,  cementum,  peridental  membrane, 

etc 482 

383.  An  infection  from  the  peridental  membrane  involving  the  medullary 

substance  in  the  cancellated  space,  an  osteomyelitis  being  the  re- 
sult  483 

384.  Destruction  of  alveolar  process  and  pi  ridental  membrane     ....     484 

385.  Destruction    of    the    alveolar    process    and    peridental    membrane    in 

pyorrhea  alveolaris 484 

386.  Absorption  of  the  apical  areas  of  the  roots  of  the  upper  central  in- 

cisors caused  by  infection 484 

387.  Eacliograms  showing  error  in  technic  of  taking 485 

S88.  Destruction  of  the  alveolar  process  and  peridental  membrane     ...      t85 

389.  Destruction   of  the   alveolar  process  and  peridental  membrane     .     .     485 

390.  Destruction    of    the    alveolar    process    and    peridental    membrane    in 

pyorrhea  alveolaris 486 

391.  Destruction  of  alveolar  process  and  peridental  membrane  in  pyorrhea 

alveolaris 486 

392.  Destruction  of  alveolar  process  and  peridental  membrane  in  pyorrhea 

alveolaris 486 

393.  Destruction  of  alveolar  process  and  peridental  membrane  establishing 

a  pocket  distal  to  the  first  molar 486 

394.  Extensive  pockets  involving  all  the  roots  of  lower  first  and  second 

molars 486 

:'.9r).  Extensive   destruction   of  alveolar   process   in   pyorrhea   alveolaris     .  1st; 

396.  Pyorrhea    alveolaris        487 

;i97.   Pyorrhea   alveolaris    in    the    lower    teeth 488 

398.  Pyorrhea  alveolaris  in  the  upper  right  cuspid 488 


ILLUSTRATIONS  1!) 

FIG.                                                                                                       •  PAGE 

399.   Pyorrhea    alveolaris       489 

4(ii).  A  typical  ease  of  pyorrhea  alveolaris 489 

101.   Destruction    of   alveolar   process   in    an   extensive   case   of   pyorrhea 

alveolaris 490 

402.  A  longitudinal  section  of  a  normal  pulp  of  man 501 

103.  Longitudinal   section   of   normal    pulp 502 

104.  Section  of  tooth  showing  relation  of  the  pulp  at  the  apical  foramen 

to    the    peridental    membrane 503 

405.    Section    <if    a    pulp    of    sheep,    showing    histologic,    characteristics    of 

odontoblastic    layer    (Color    Plato) 504 

-10G.   Secondary    dentin 512 

407.  Secondary  dentin  which  entirely  filled  the  pulp  chamber     ....  .11.'! 

408.  Secondary  dentin   in  connection  with  abraded  upper  central     .     .     .  513 

409.  Secondary  dentin  in  connection  with  severe  abrasion 513 

410.  Pulp  the  seat  of  a  chronic  inflammation 513 

411.  Chronic  inflammation   of   the   pulp 511 

412.  Pulp  stones  occupying  the  entire  pulp  chamber 515 

41."..  Pulp  stone   (nodule)   in  pulp  chamber  of  lower  molar 515 

!14.  Pulp  nodule  filling  up  the  entire  pulp  chamber 515 

-J  15.  A    pulp    nodule    in    situ 515 

416.  Decalcified  section  with  pulp   stone   in   situ 516 

417.  Decalcified   longitudinal   section,   showing   pulp   stone   in   place     .     .  51G 

418.  Pulp  stones  in  situ    (Color  Plate) 516 

419.  Pulp   stones   in   situ    (Color   Plate) 516 

420.  Pulp  stones  in  pulp  chamber  of  upper   right   first  and  second  molars  517 

421.  Section    of    dental    pulp,    longitudinal 519 

422.  Cross  section   of   hyperemie  pulp 520 

423.  Longitudinal   section  of  a   dental  pulp,  the  upper  portion  of  which 

has   beL'n   the    seat   of   suppuration 529 

424.  Simple    cyst 533 

4  25.  Adamantinoma 536 

4  26.  Roentgenogram  showing  entire  absence  of  ramus  of  jaw  on  right  side 

and  tumor  extending  across  midline  to  bicuspid  region  on  left  side  537 

427.  Adamantinoma 539 

428.  Adamantinoma 540 

429.  Section    of    adamantinoma 541 

430.  Section    of    adamantinoma 541 

431.  Section    of    adamantinoma 542 

432.  Cystic     cavities    in     adamantinoma 542 

433.  Portion  of  a  mandible  with  cortical  layer  of  bone  removed     .     .     .  545 

434.  Vertical  gross  section  of  mandible  in  molar  region 546 

435.  Decalcified  transverse  section  of  upper  central  incisors 546 

436.  Radiograph    of    case    of    systemic    involvement ~<~>~> 

437.  Radiograph    of    case    of   systemic    involvement 556 

438.  Eadiograph   of  case   of  systemic   involvement 557 


20 


ILLUSTRATIONS 


FIG.  PAGE 

439.  Radiograph  of   case   of   systemic   involvement 558 

440.  Eadiograph  of   case   of   systemic   involvement 558 

441.  Radiograph  of   case    of   systemic   involvement 559 

442.  Radiograph  of   case    of   systemic    involvement 560 

443.  Radiograph  of   case   of   systemic   involvement 560 

444.  Ulcerative  stomatitis     (Color    Plate) 5G8 


GENERAL  AND  DENTAL  PATHOLOGY 


PART  I 
GENERAL  PATHOLOGY 


CHAPTER  I 

INTRODUCTORY 

Pathology  is  the  science  which  treats  of  the  causes,  manifesta- 
tions, and  results  of  disease.  Broadly  speaking,  pathology  stud- 
ies disease  in  all  its  phases,  but  the  bulk  of  the  clinical  symp- 
toms and  the  treatment,  which  constitute  so  large  a  field  of  in- 
vestigation, are  usually  dealt  with  in  other  departments  of  medical 
science. 

Disease1  is  any  alteration  of  the  structure  or  the  composition 
of  the  tissues,  which  impairs  or  tends  to  impair  their  function.2 
Disease  is  not  an  established  entity,  but  a  process.  It  is  a  continu- 
ing series  of  alterations  which  go  on  until  interrupted  by  death, 
or  until  recovery  takes  place.  The  examination  of  a  pathologic 
specimen  shows  the  changes  in  structure  and  composition  which 
have  taken  place  up  to  the  time  when  the  tissue  was  examined; 


'It  is  often  contended  that  disease  can  not  be  accurately  or  scientifically  defined,  that 
there  is  no  clearly  marked  dividing  line  between  health  and  disease.  This  is  undoubtedly 
true,  but  the  same  objection  obtains  against  a  definition  of  insanity,  abnormality,  hys- 
teria, death  and  many  other  terms.  Eut  few  terms  could  be  defined,  if  an  absolutely  un- 
assailable and  faultless  definition  were  demanded.  A  definition  that  would  include  all  path- 
ologic manifestations  and  exclude  all  normal  variations  is  neither  possible  nor  necessary. 
It  is  far  more  important  that  the  general  reader,  and  particularly  the  student  who  is  just 
beginning  the  study  of  pathology,  should  learn  the  meaning  of  terms  as  they  are  generally 
used  and  understood  by  pathologists,  than  that  our  definition  should  be  scientifically 
flawless. 

:"Just  as  physiology  is  the  study  of  the  functions  of  the  body  in  health,  so  is  pathology 
the  study  of  the   same  functions  in  disease." — Adami. 

"*     *     *     disease  is  not  a  thing,  but  a  process.     It  is  an  abnormal  performance  of  cer- 
tain  of  the  functions  of  the  body." — Delafield  snd  Prudden. 

"It  is  doubtful  whether  alterations  of  function  can  occur  without  some  alteration  in 
structure." — Stengel   and   Fox. 

21 


22  GENERAL   PATHOLOGY 

later  examinations  will  reveal  furl  her  alterations,  and  in  many 
instances  additional  pathologic  processes. 

Health  is  that  state  or  condition  in  which  the  tissues  and  organs 
of  the  body  are  enabled  to  perform  all  their  functions  in  a  normal 
manner.  It  is  of  course  impossible,  with  any  great  degree  of 
exactitude,  to  point  out  where  normality  ends  and  abnormality 
begins,  so  gradually  does  the  one  condition  merge  into  the  other. 
The  nearer  we  approach  the  boundary  line,  the  more  difficult  it 
becomes  to  determine  whether  we  are  face  to  face  with  a  normal 
variation  of  health  or  incipient  disease.  This  difficulty,  how- 
ever, disappears  when  a  well-marked  instance  of  disease  is  met 
with,  and  the  task  then  resolves  itself  into  a  determination  of 
the  nature  and  extent  of  the  morbid  process. 

Health  then  is  the  performance  of  all  the  functional  activities 
of  the  body  in  a  normal  (i.e.,  an  average,  regularly  established) 
manner,  and  disease  is  impairment  of  these  activities.  In  those 
cases  where  function  is  pathologically  increased,  as  in  the  hy- 
pertrophies, the  increase  is  at  most  only  temporary  and  tends 
toward  impairment  later;  in  fact,  when  considered  as  a  part  of 
the  sum  total  of  activities  which  must  act  in  harmony  to  con- 
stitute a  state  of  health,  any  pathologic  increase  of  functional 
activity  must  be  regarded  as  an  impairment  of  health. 

Life  and  functional  activity  are  one  and  the  same  thing.  Let 
one  of  the  vital  organs  cease  to  do  its  work  and  death  ensues. 
So  far  as  biological  science  can  determine,  life  is  the  result  of 
chemical  (more  correctly,  physicochemical)  processes  occurring 
within  the  tissues.  When  these  processes  are  so  coordinated 
that  all  the  organs  perform  their  activities  in  perfect  harmony 
with  one  another,  the  individual  is  said  to  be  healthy;  when  these 
processes  are  stimulated  or  retarded,  by  any  cause  whatsoever, 
beyond  the  normal,  disease  results.  These  abnormal  chemical 
changes  in  the  tissues  can  often  be  demonstrated  by  means  of 
staining  and  other  reactions  before  structural  changes  manifest 
themselves,  and  in  all  cases  precede  the  latter.  Chemical  and 
structural  changes  result  in  changes  of  function,  that  is,  disease. 
The  so-called  "functional  diseases"3  as  for  example,  epilepsy,  are 
such  as  exhibit  decided  functional  changes,  without  discoverable 


3Green's   Pathology,  p.   5. 


INTRODUCTORY  '2'.) 

anatomic  or  chemical  changes,  bu1   these  undoubtedly  exisl   and 
have  caused  the  functional  disturbance. 

Pathology  therefore  studies  the  morbid  side  of  anatomy,  chemis- 
try, and  physiology,  and  it  follows  that  a  comprehensive  knowledge 
of  normal  anatomy,  chemist vy,  and  physiology  is  a  prerequisite  to 
the  study  of  pathologic  conditions. 

THE  CELL 

The  living  organism,  animal  and  vegetable,  is  made  up  wholly 
of  cells.  Although  recognized  much  earlier,  the  cell  was  not  gen- 
erally accepted  as  the  structural  unit  until  Virchow  founded 
modern  pathology  by  the  publication  of  his  epochal  work  on 
Cellular  Pathology  in  1858.  Since  then  it  has  also  become  the 
basis  of  chemical  and  physiologic  considerations,  and  the  cell  is 
now  the  histologic,  the  chemical  and  the  physiologic  or  biological 
unit. 

All  organisms,  unicellular  and  multicellular,  are  derived  from 
a  parent  cell  ("omnis  cellula  e  cellula"- — Virchow).  The  uni- 
cellular organisms,  as  protozoa  and  bacteria,  are  composed  of 
but  one  cell,  which  is  capable  of  performing  all  the  essential  vital 
functions.  In  the  multicellular  organisms,  the  cells,  after  a  suffi- 
cient number  have  been  formed  from  the  parent  cell,  form  groups 
which  become  differentiated  during  the  course  of  the  development 
of  the  embryo,  and  destined  to  perform  different  functions.  Such 
differentiated  or  specialized  groups  of  cells  with  their  character- 
istic intercellular  substance  (the  latter  being  in  all  instances  a 
product  of  the  cells  themselves)  constitute  the  various  tissues; 
appropriate  amounts  and  kinds  of  different  tissues  form  organs; 
and  a  system  of  organs  with  their  supporting  structures  form 
the  individual  organism. 

Protoplasm  is  a  term  given  to  the  albuminous  material  which 
composes  the  cell  and  gives  to  it  its  vital  properties.  It  is  not 
synonymous  with  cytoplasm  (q.v.)  or  any  histologic  division  of 
the  cell.  It  is  the  basic  substance  found  in  all  parts  of  the  cell. 
Structurally  the  cell  may  be  divided  into  two  essential  parts — 
the  cytoplasm  and  the  nucleus.  Given  these  two  essentials,  a 
cell  can  perform  all  its  physiologic  functions,  and  may  there- 
fore be  considered  a  true  cell.  In  addition  to  these  two  parts, 
the  vegetable  cells  and  some  of  the  animal  cells  have  a  peripheral 


24  GENERAL   PATHOLOGY 

membrane,  or  cell  wall ;  and  some  cells,  particularly  when  in  an 
actively  reproducing-  state,  contain  a  body  called  the  centrosome. 
A  typical  cell,  therefore,  may  be  said  to  consist  of  the  follow- 
ing structures: 

Anatomy  of  the  Cell 

1.  A  cell  wall,  or  membrane. 

2.  Cytoplasm,   or  cell  material  exclusive   of  the  nucleus. 

3.  The  nucleus,  or  karyon  (literally,  a  nut  or  kernel). 

4.  Centrosome,  lying  within  its  centrophere. 

The  cell  wall,  or  membrane  is  a  condensation  and  modification 
of   the   peripheral   cytoplasm,   which   governs   the   entrance   and 


Fig.  '1. — Diagram  of  a  typical  cell.  (After  Bailey.)  /,  Cell  membrane;  2,  metaplasm; 
.?.  karyosome;  4,  hyaloplasm;  5,  spongioplasm;  6,  linin;  7,  nucleoplasm;  S,  attraction 
sphere;  9,  centrosome;  10,  plastids;  //,  chromatin  network;  12,  nuclear  membrane;  13; 
nucleolus;    14,   vacuole. 

exit  of  nutritive  substances  excretory  products  and  other  ma- 
terials. Only  a  few  of  the  animal  cells,  such  as  fat  cells,  goblet 
cells,  cartilage  cells,  etc.,  have  a  distinct  cell  wall ;  the  great 
majority  of  animal  cells  present  merely  a  more  or  less  homo- 
geneous outer  layer  of  cytoplasm,  called  ectoplasm  or  exoplasm, 
to  distinguish  it  from  the  inner  endoplasm  which  is  usually  granu- 
lar, and  the  phenomena  of  diffusion  and  osmosis  indicate  that 
the  ectoplasmic  zone  serves  the  purposes  of  a  cell  wall. 

Vegetable  cells  have  distinct  cell  walls,  which  often  contain 
cellulose  or  chitin.  The  former  appears  as  a  blue  circle  on  the 
application  of  iodine. 


INTRODUCTORY  -•> 

The  cytoplasm,  or  cell  body,  is  a  semifluid  substance  composed 
of  a  network  of  fibrils  (cytoreticulum)  called  spongioplasm,  in  the 
meshes  of  which   is  found  a  clear,  glass-like,   homogeneous,  semi 
fluid  substance  called  hyaloplasm  (also  paraplasm). 

The  actual  structure  of  the  spongioplasm  is  still  a  mooted  ques- 
tion. Altmann  believed  it  to  be  made  up  of  granules  lying  in  a 
gelatinous  substance,  lie  believed  these  granules  to  be  the  vital 
elements  of  the  cell  and  called  them  bidblasts.  Butchli's  "foam" 
theory  considers  the  reticular  appearance  of  the  spongioplasm  to 
be  due  to  a  foam-like  emulsion  produced  by  the  mixture  of  fluid 
of  different  degrees  of  viscosity,  the  cut  walls  of  the  minute 
foam  spaces  resembling  a  network.  Others  still  believe  the 
spongioplasm  to  be  a  felt  work  of  independent  fibrils  (filar  mass 
or  mitome). 

Within  the  cytoplasm  are  often  found  granules  of  pigment  or 
secretory  products,  fat  globules,  substances  in  vacuoles,  etc., 
which  are  collectively  called  metaplasm  or  paraplasm  (though 
some  writers  use  the  latter  term  as  synonymous  with  hyaloplasm). 
These  cell  inclusions  are  adventitious  bodies  and  not  true  con- 
stituents of  the  cell. 

Plastids  or  protoplasts  are  bodies  often  occurring  in  vegetable 
cells,  less  often  in  animal  cells,  which  are  usually  regarded  as 
local  areas  of  cytoplasm,  specialized  for  the  performance  of  some 
function,  e.g..  the  transformation  of  starch,  etc. 

The  nucleus  is  a  vesicular  body,  which  in  general  conforms  to 
the  shape  of  the  cell,  being  elongated  in  muscle  and  connective 
tissue  cells,  flat  in  epithelial  cells,  etc.  Its  morphology,  however, 
may  be  very  irregular,  as  seen  in  leucocytes,  and  the  large  bone- 
marrow  cells  (megakaryocytes) .  The  typical  cell  contains  but  one 
nucleus,  while  the  osteoclasts  and  the  various  giant  cells  are  mul- 
tinucleated, resulting  probably  from  repeated  division  of  the 
nucleus  without  corresponding  division  of  the  cytoplasm. 

The  vegetative  nucleus  (one  not  in  active  process  of  division) 
has  a  transparent,  faintly  staining  nuclear  wall  or  membrane 
(amphipyn  nin). 

The  substance  of  the  nucleus,  or  karyoplasm  structurally  re- 
sembles the  cytoplasm  in  being  composed  of  a  network  of  fibrils 
(nucleoreticulum)  and  an  interfibrillar  semifluid  material  (nucleo- 
plasm, nuclear  matrix). 


26  GENERAL   PATHOLOGY 

The  nucleoreticulum  consists  of  an  achromatic,  faintly  staining 
network  of  fibrils  (or  linin),  which  supports  in  its  meshes  a  deeply 
staining  substance,  called  chromatin  because  of  its  great  affinity 
for  basic  dyes.  At  the  nodal  points  of  the  linin,  the  accumula- 
tions of  chromatin  into  conspicuous  granules  are  called  karyo- 
somes  (or  net  knots  or  false  nucleoli).  As  usually  stained  the 
nuclei  of  many  cells  appear  to  be  composed  almost  solidly  of 
chromatin,  because  the  latter  stains  deeply,  while  the  linin  and 
nucleoplasm  stain  faintly. 

The  nucleoplasm  or  matrix  is  a  clear  fluid  or  semifluid  sub- 
stance, lying  in  the  meshes  of  the  nucleoreticulum,  probably  nu- 
trient in  character,  resembling  the  hyaloplasm  of  the  cytoplasm. 

The  nucleolus,  or  plasmosome,  is  a  small  spherical  body,  some- 
times more  than  one.  lying  within  the  nucleus.  It  does  not  ap- 
pear to  be  attached  to  the  nuclear  structures,  stains  less  in- 
tensely than  the  chromatin,  particularly  in  fixed  tissues,  where  it 
elects  the  acid  stains,  resembling  in  this  respect  the  cytoplasm. 
Its  function  is  not  known. 

Cells  without  nuclei,  as  the  red  blood  cells,  are  no  longer  true 
or  complete  cells,  having  lost  the  nuclei  which  all  such  cells  pos- 
sessed in  their  early  life  history,  together  with  their  power  of 
reproduction. 

In  some  of  the  simple  forms  of  life,  as  bacteria,  the  nucleus 
either  fills  the  whole  cell,  leaving  an  almost  undemonstrably 
small  ring  of  cytoplasm  about  the  nucleus;  but  according  to  the 
more  generally  accepted  view,  the  nuclear  material,  instead  of 
being  collected  together  into  a  compact  nuclear  body,  is  scat- 
tered throughout  the  entire  cell.  Bacterial  cells,  therefore,  re- 
semble the  nuclei  of  tissue  cells  in  staining  solidly  and  in  hav- 
ing the  same  affinity  for  basic  dyes. 

The  centrosome  is  a  very  minute  body  of  variable  staining 
quality,  and  often  difficult  to  distinguish  from  metaplasmic  gran- 
ules. It  is  usually  found  in  the  cytoplasm  near  the  nucleus,  and 
is  often  surrounded  by  a  clear  area,  the  ccntrosphere,  from  which 
radiations  into  the  surrounding  cytoplasm  may  be  seen  when  the 
cell  is  about  to  divide. 

The  Chemistry  of  the  Cell 

Protoplasm,  or  bioplasm,  is  the  soft,  colorless,  jelly-like  sub- 
stance of  which  living  cells  or  tissues  are  composed.     There  is 


INTR0D1  CTORY  27 

no  way  of  chemically  analyzing  living  protoplasm.  Chemical 
reagents  cause  the  death  of  the  cells  with  coagulation  of  various 
constituents,  etc.,  hence  the  term  "protein"  (given  to  the  most 
important  constituent  of  protoplasm)  refers  necessarily  1o  what 
the  chemist  finds  when  he  analyzes  dead  cells,  while  the  term 
"proteinogen"  may  be  applied  to  the  living  material. 

Thus  analyzed,  cells  are  found  to  he  composed  essentially  of 
proteins,  lipoids,  inorganic  suits  and  watt  r,  often  called  the  primary 
constituents.  Other  substances  as  fats,  carbohydrates,  secretory 
granules,  pigment  granules,  enzymes,  etc.,  are  food  mate- 
rials and  metabolic  products,  and  are  not  essential  chemical  com- 
ponents of  the  cell.  These  are  often  called  secondary  constit- 
uents, and  it  is  these  secondary  constituents  that  account  for 
the  great  differences  in  the  histologic  appearances  of  the  various 
types  of  cells. 

Proteins  are  the  most  complex  substances  known  to  the  chemist. 
They  will  not  diffuse  through  animal  membranes  or  other  dif- 
fusion membranes,  and  some  fail  even  to  pass  through  fine  porce- 
lain filters,  hence  their  molecules  must  be  very  large.  Both  their 
structural  and  molecular  formula?  are  as  yet  unknown,  and  even 
their  empiric  or  percentage  formulae  have  only  been  approxi- 
mately determined.  For  example,  the  percentage  composition 
of  oxyhemoglobin  (one  of  the  simplest  of  the  proteins)  varies 
according  to  different  analyses;  perhaps  the  most  trustworthy 
being  C658H1181O210N207S2Fe ;  while  the  molecular  weight  accord- 
ing to  different  reports  varies  from  15,000  to  17,000. 

By  hydrolysis  of  the  proteins,  with  acids,  alkalies,  steam  or 
enzymes,  they  yield  successively,  although  not  wholly  synchron- 
ously, proteoses,  peptones  and  peptides  (which  still  retain  certain 
properties  characteristic  of  proteins)  and  finally  amino  acids— 
the  "building  stones"  or  ultimate  constituents  of  the  protein 
molecule.  These  amino  acids  are  optically  active,  crystalloid  sub- 
stances, of  known  chemical  structure.  Each  contains  an  acid 
(carboxyl)  group  and  a  basic  (amin)  group,  and  is  therefore  am- 
photeric in  reaction.     Their  type  formula  is 

NIL  O 

I     "    II 
R— CH— C— O— H 


28  GENERAL   PATHOLOGY 

Eighteen  of  these  acids  have  been  identified;  all  contain  the 
ammo-acid  radicle  combined  with  other  groups  or  "nuclei,"  and 
the  latter  may  belong  to  the  aliphatic,  or  open-chain  series  (as 
glycocoll),  homocyclic  (as  tyrosin)  or  heterocyclic  (as  trypto- 
phane). 

All  protein  food  materials  are  reduced  by  the  digestive  enzymes 
into  amino  acids,  preparatory  to  assimilation  by  the  cell;  after 
their  introduction  into  the  cell,  the  amino  acids  are  synthesized 
by  the  intracellular  enzymes  into  such  type  of  proteins  as  the 
cells  may  need. 

Proteins  have  been  classified  as  follows  :4 

I.  Simple  Proteins.  Substances  which  yield  only  amino  acids 
on  hydrolysis. 

(a)  Albumins,  as  egg  albumin,  serum  albumin,  lactalbumin. 

(b)  Globulins,   as   serum   globulin,   ovoglobulin    (from   yolk   of 

cfeO  )  ' 

(c)  Glutelins,  as  glutenin  from  wheat. 

(d)  Prolamins,  as  hordein  from  barley. 

(e)  Albuminoids  or  scleroproteins,  as  collagen,  elastin  and 
keratin,  from  fibrous  tissues,  elastic  tissues  and  skin  appendages 
respectively. 

(f)  Histones,  as  globin  from  hemoglobin. 

(g)  Protamins,  the  simplest  natural  proteins,  as  salmine. 

The  simple  proteins  differ  among  themselves  in  solubility, 
coagulability  and  other  properties. 

II.  Conjugated  or  Compound  Proteins. 

(a)  Nucleoproteins.  Compounds  of  protein  molecules  and  nu- 
cleins.  The  nueleins  yield  on  further  hydrolysis  other  protein 
molecules  and  nucleic  acids.  Nucleic  acids  are  rich  in  phosphorus, 
being  composed  of  phosphoric  acid,  pyrimidin  bases,  purin  bases 
("nuclein  bases")  and  a  carbohydrate.  The  different  combina- 
tions of  these  various  ingredients  result  in  an  enormous  variety 
of  nucleoproteins,  which  constitute  the  most  important  part  of 
the  cell,  both  of  cytoplasm  and  nucleus. 

(b)  Glycoproteins.  Compounds  of  protein  molecules  and  a  car- 
bohydrate group  (other  than  that  present  in  the  molecule  of  nu- 
cleic acid),  as  the  mucin  of  secretory  cells,  and  the  mucoid  of 
fibrous  tissues. 


4The   American    Physiological   Society   and   The   American    Society   of    Biological    Chem- 
ists. 


[NTRODUCTOR'S  29 

(e)  Phosphoproteins.  Compounds  of  protein  and  phosphorus- 
containing  substances  (other  than  nucleic  acid  or  lecithin),  as 
casein  from  milk. 

(d)  Hemoglobins.  Compounds  of  protein  with  hematin  or  simi- 
lar substance,  as  hemoglobin  from  blood. 

(e)  Lecithoproteins.  Compounds  of  protein  with  lecithins  (see 
below). 

Lipoids  are  substances  which  resemble  fats  in  certain  physical 
properties  but  differ  chemically;  they  dissolve  in  ordinary  fat 
solvents.  The  chief  lipoids  (or  "fat-like"  bodies)  are  lecithin 
and  cholesterin. 

Lecithin  is  a  combination  of  certain  fatty  acid  radicals  with  phos- 
phoric acid  and  cholin,  and  constitutes  the  greater  part  of  the 
lipoids.     Lecithin  plays  a  very  important  part  in  cell  metabolism. 

Cholesterin,  or  cholesterol,  is  an  alcohol,  related  to  the  terpenes. 
It  is  chemically  rather  inert,  and  its  role  is  probably  a  physical 
one. 

Inorganic  Salts,  particularly  chlorides,  carbonates,  phosphates, 
and  sulphates  of  the  alkaline  metals  and  the  alkaline  earths, 
ionize  in  the  water  of  the  cell,  and  their  ions  unite  chemically 
with  the  protein  groups  (ion  proteins).  It  is  very  probable  that 
proteins  and  lipoids  engage  in  those  chemical  reactions,  which 
are  essentially  the  basis  of  life,  only  as  they  form  compounds 
with  the  ions  of  inorganic  salts. 

Water  in  generous  amount  within  the  cell  is  necessary  to  carry 
out  the  vital  chemical  processes,  because  it  is  the  medium  in 
which  dissociation  of  the  molecules  of  the  salts  above  mentioned 
may  take  place,  and  the  ions  which  are  constantly  liberated  and 
reunited  during  the  life  of  the  cell  become  the  electrolytes,  bear- 
ing the  electrical  charges  or  energies  which  represent  the  fun- 
damental vital  processes. 

The  Physics  of  the  Cell 

The  substances  before  mentioned  as  essential  or  primary 
chemical  constituents  of  the  cell,  together  with  the  secondary 
constituents,  are  present  in  different  physical  states ;  viz.,  as 
colloids  and  crystalloids  which  are  in  solution,  or  semisolution,  in 
the  water  and  in  each  other. 


30  GENERAL    PATHOLOGY 

It  should  be  borne  iu  mind  that  a  solution  is  a  physical  condi- 
tion— a  homogeneous  mixture  of  molecules,  and  that  ionization  is 
an  additional  process  whereby  the  molecules  which  have  undergone 
solution  are  to  a  greater  or  less  degree  dissociated  into  atoms  or 
groups  of  atoms  electrically  charged.  When  acids,  bases,  and  salts 
"dissolve"  in  water,  there  is  solution  plus  ionization.  A  sus- 
pension or  emulsion  is  a  more  or  less  homogeneous  mixture  of  mi- 
nute masses  of  molecules  in  a  fluid. 

Colloids  are  substances  which  do  not  pass  through  diffusion  mem- 
branes or  do  so  very  slowly.  They  are  usually  amorphous,  but 
hemoglobin,  egg  albumin  and  certain  other  proteins  crystallize 
readily.  Colloids  include  all  forms  of  proteins,  the  carbohy- 
drates (except  the  sugars),  tannic  acid,  etc.,  also  various  in- 
organic compounds  and  metals.  The  protein  colloidal  solution 
is  either  a  true  solution  of  protein  molecules,  whose  size,  though 
undetermined,  must  be  very  great;  or,  as  is  more  generally  be- 
lieved, it  is  a  suspension  of  minute  masses  of  protein  molecules. 
The  colloids  within  the  cell  are  therefore  believed  to  be  in 
a  state  of  suspension.  The  foodstuffs  of  the  cells — proteins,  car- 
bohydrates and  fats — in  colloid  form  are  first  reduced  to  the 
crystalloid  form  of  amino  acids,  sugar  and  diffusible  soaps  and 
glycerin  respectively,  and  when  these  enter  the  cell  through  the 
cell  wall,  which  acts  as  a  diffusion  membrane,  pervious  to  water, 
salts,  and  crystalloids,  but  impervious  to  colloids,  they  are  syn- 
thesized into  colloidal  proteins,  fats,  and  carbohydrates  again 
by  aid  of  the  intracellular  enzymes. 

Crystalloids  are  substances  which  diffuse  readily  through  the 
usual  diffusion  membranes,  and  tend  to  form  crystals  under 
favorable  conditions.  The  cellular  crystalloids  include  inorganic 
salts,  sugars,  amino  acids,  urea,  creatinine,  etc.  The  inorganic 
crystalloids  or  salts  form  ions,  which  carry  electric  charges 
and  are  therefore  electrolytes.  The  organic  crystalloids  do  not 
ionize  and  are  nonelectrolytes.  As  Mann  had  stated,  the  elec- 
trolytes put  life  into  the  proteins.  The  organic  crystalloids  are 
chiefly  important  as  foods  or  metabolic  products. 

Staining  Reactions  of  the  Cell 

The  cell  protoplasm  consists  largely  of  nucleoproteins. 

In  the   cytoplasm   all  the   primary   constituents  already  men- 


INTRODUCTORY  31 

tioned  are  present,  as  well  as  manj  of  the  secondary  constituents, 
lull  the  rmcleoproteins  predominate,  and  consisl  of  nucleic  acid 
well  saturated  with  protein  materials,  thus  permitting  t  lie  reac- 
tion of  the  cytoplasm  as  a  whole  to  be  neutral  or  slightly  alkaline, 
in  which  condition  it  naturally  elects  the  acid  stains. 

The  nucleus  is  very  largely  composed  of  nucleoprotein,  but  the 
nucleic  acid  portion  of  the  molecule  is  not  so  "well  saturated  with 
protein  as  in  the  cytoplasm,  and  the  nucleus  as  a  whole  is  acid 
in  reaction  and  elects  the  basic  stains.  Because  the  unsaturated 
nucleoprotein  stains  so  readily  and  intensely,  it  is  called  chro- 
matin.  When  the  nucleus  is  in  the  process  of  mitotic  division, 
the  nucleic  acid  portion  of  the  chromatin  (nucleoprotein)  becomes 
still  less  saturated  than  when  in  the  resting  or  vegetative  state, 
hence  stains  more  intensely. 

The  linin,  as  well  as  the  nucleolus,  is  composed  of  well-satu- 
rated nucleoproteins,  and  therefore  resembles  the  cytoplasm  in 
staining  reactions. 

The  staining  reagents  most  commonly  used  are  the  anilin  dyes, 
manufactured  from  coal  tar,  and  are  derivatives  of  benzene  and 
its  homologues.  Some  of  these  stains  are  acid,  others  basic  in 
reaction,  and  require  the  opposite  reaction  in  the  tissues  in  order 
to  stain  well. 

The  tissue  elements  may  be  classified  into: 

(a)  Oxyphillic,  acidophillic  or  eosinophillic,  which  comprise  the 
cytoreticulum,  centrosomes,  attraction  spheres,  nuclear  mem- 
branes, linin,  nucleoli  and  certain  cytoplasmic  granules.  The 
general  normal  reaction  of  these  elements  is  slightly  alkaline. 

The  more  important  of  the  acid  or  cytoplasmic  dyes  are  eosin, 
erythrosin  and  acid  fuchsin. 

(b)  Basophillic,  which  comprise  the  substances  rich  in  nucleic 
acid  as  chromatin  and  certain  cytoplasmic  granules  (other  than 
those  already  mentioned). 

The  more  commonly  used  of  the  basic  dyes  are  hematoxylin, 
methylene  blue,  gentian  violet,  thionin  blue,  Bismarck  brown  and 
basic  fuchsin. 

(e)  Some  tissue  elements  have  the  power  of  combining  with, 
or  absorbing  either  acid  or  basic  dyes,  and  are  therefore  called 
amphophillic. 


32  GENERAL    PATHOLOGY 

(d)  Other  elements,  again,  are  stained  by  the  neutral  salt  dyes, 
as  the  eosinate  of  methylene  blue  (Romanowski)  and  the  triple 
stain  of  Ehrlich.  The  fine  granules  of  the  polymorphonuclear 
leucocytes  are  neutrophillic. 

The  Physiology  of  the  Cell 

All  true  cells  (or  those  which  have  nuclei)  have  the  funda- 
mental properties  of  nutrition,  growth,  irritability,  motility  and 
reproduction. 

Nutrition. — The  cell  is  able  to  receive  food  substances  from  with- 
out and  transform  them  into  living  protoplasm  (andbolism)  ;  also 
to  break  down  old  and  worn  protoplasm  into  waste  products  (ca- 
tabolism),  and  extrude  these  from  the  cell.  The  sum  total  of  these 
anabolic  and  catabolic  chemical  processes  is  called  metabolism. 

Growth,  or  increase  in  size  of  the  cell,  is  a  natural  consequence 
of  nutrition,  and  is  due  to  greater  activity  on  the  part  of  the 
anabolic  than  of  the  catabolic  processes. 

Irritability. — This  is  a  definite  response  to  external  stimuli. 
The  character  of  the  response  depends  upon  the  nature  of  the 
protoplasm ;  the  muscle  cell  contracts,  the  glandular  epithelium 
secretes,  and  the  nerve  cell  conveys  impulses. 

Motility  is  the  power  of  executing  spontaneous  movements  and 
is  exhibited  in  different  forms : 

(a)  Protoplasmic  movement,  which  is  an  intracellular  move- 
ment as  shown  by  the  circulation  or  "streaming"  of  the  pro- 
toplasm. The  minute  granules,  the  nucleus,  and  other  constit- 
uents move  about,  though  in  a  restricted  manner  within  the 
living  cell. 

(b)  Ameboid  movement  is  a  similar  but  more  specific  move- 
ment on  the  part  of  the  protoplasm,  consisting  of  a  protrusion  of 
certain  parts  of  the  cell  (pseudopodia)  beyond  its  usual  outline. 
These  pseudopodia  may  retract  or  may  proceed  until  the  whole 
cell  has  been  drawn  after  them,  changing  both  the  shape  and 
the  position  of  the  cell. 

(c)  Ciliary  movement  is  the  wave-like  motion  of  minute  hair- 
like extensions  of  specialized  cytoplasm,  called  cilia.  Only  the 
columnar  variety  of  epithelium  is  ciliated.  A  cell  may  have 
from  one  to  two  dozen  cilia. 


INTRODUCTORY  '■'>'■'> 

Iii  all  cases  of  cellular  motion  resulting  in  a  change  of  shape  of 
the  cell,  as  in  ameboid  and  ciliary  motion,  and  in  functionating 
muscle  cells,  il  is  the  spongioplasm  which  contracts;  the  hy- 
aloplasm plays  only  a  passive  role  and  is  believed  to  represent 
nutritive  material. 

Reproduction  is  the  derivation  of  one  or  more  cells  from  a 
parenl  cell.  Cel]  reproduction  occurs  in  one  of  two  ways— by 
direct  cell  division  and  by  indirect  division. 

Tn  the  direct  form,  amitosis,  Hie  nucleus  divides  withoul  any 
demonstrable  preliminary  changes  in  its  histology.  This  method 
of  division  is  common  in  protozoa  and  other  lower  forms  of  life. 

In  the  indirect  cell  division,  mitosis  or  Tcaryokinesis,  the  nucleus 
passes  through  certain  complex  changes,  and  these  changes,  to- 
gether with  alterations  of  other  constituents  of  the  cell,  are  usu- 
ally described  as  taking  place  in  the  following  stages  or  phases: 

The  Prophase,  in  which  changes  preparatory  to  division  occur. 

The  chromatin  network  is  formed  into  one  or  more  threads 
(skein  or  spireme),  which  later  divides  into  segments  (chromo- 
somes), the  number  of  which  is  fixed  and  definite  for  each  species 
of  plant  or  animal  cell. 

The  centrosome  develops  a  distinct  attraction  sphere  and  di- 
vides into  two  "stars"  or  asters,  which  separate,  going  to  oppo- 
site poles  of  the  cell,  but  still  connected  by  fibrils  of  linin 
(achromatic  spindle).  The  chromatin  segments  arrange  them- 
selves along  the  equatorial  line  of  the  spindle. 

The  nuclear  membrane  and  nucleolus  disappear  during  this 
phase. 

The  Metaphase,  in  which  actual  division  of  the  nucleus  occurs. 

Each  chromosome  (or  segment  of  chromatin)  splits  longi- 
tudinally, forming  daughter  chromosomes. 

The  Anaphase,  in  which  the  changes  are  in  the  main  the  re- 
verse of  those  occurring  in  the  prophase. 

The  daughter  chromosomes  separate,  one-half  going  to  one  pole 
along  the  linin  threads  of  the  achromatic  spindle,  the  other  half 
going  to  the  opposite  pole,  where  they  form  daughter  nuclei. 

The  Telophase,  the  finishing  stage,  in  which  the  cell  body  di- 
vides at  right  angles  to  the  axis  of  the  spindle  into  two  cells,  each 
now  having  received  an  equal  portion  of  the  nucleus  and  one 


GENERAL    PATHOLOGY 


of  the  newly  formed  eentrosomes.  A  nuclear  membrane  and  a 
nucleolus  appear  in  each  new  cell.  Nothing  is  at  present  known 
regarding  the  function  of  the  nucleolus.     (Fig.  2.) 


Fig.    2. — Diagrams    of    successive    phases    of    mitosis. 

A.  Resting  cell,  with  reticular  nucleus  and  true  nucleolus;  c,  attraction  sphere  with 
two    eentrosomes. 

B.  Early  prophase.  Chromatin  forming  continuous  thread — the  spireme;  nucleolus 
still  present;  a,  amphiaster;  the  two  eentrosomes  connected  by  fibrils  of  achromatic 
spindle. 

C.  Later  prophase.  Segmentation  of  spireme  to  form  the  chromosomes;  achromatic 
spindle    connecting   eentrosomes;    polar    rays;    mantle    fibers;    fading   of   nuclear   membrane. 

D.  End  of  prophase.  Monaster — mitotic  figure  complete;  cp,  chromosomes  arranged 
around  equator  of  nucleus;  fibrils  of  achromatic  spindle  connecting  eentrosomes;  mantle 
fibers   passing   from   eentrosomes    to    chromosomes.      (E.    B.    Wilson,    "The    Cell.") 


Origin  of  the  Blastodermic  Layers 

The  matured  ovum,  after  union  with  the  spermatozoon  has  oc- 
curred {fertilization),  enters  upon  a  series  of  repeated  divisions 
{segmentation) .  The  first  result  is  a  solid  spherical  mass  of  cells 
{morula).  This  mass  soon  forms  a  cavity  in  its  center,  which 
grows  until  there  is  a  hollow  sphere  (the  blastodermic  vesicle)  sur- 
rounded bv  a  single  layer  of  cells  attached  to  the  inner  surface 


IN'TK HiiKV 


35 


of  the  vesicle  excepl  a1  one  point  of  the  inner  surface  where  a 
small  mass  of  cells  persists  which  is  called  the  embryonic  area, 
because  it   is  in  this  small  mass  of  cells  that  the  future  embryo 


Fig.    2. — Diagrams    of    successive    phases    of    mitosis. 

E,  Metaphase.      Longitudinal    cleavage;    splitting    of    chromosomes    to    form    daughter 
chromosomes,   ep;   n,   cast-off   nucleolus. 

F,  Anaphase.     Daughter  chromosomes  passing  along  fibrils  of  achromatic  spindle  toward 
centrosomes;   division   of   centrosomes;    if,   interzonal   fibers   or   central   spindle. 

G,  Late  anaphase.     Formation  of  diaster;  beginning  division  of  cell  body. 

H.   Telophase.       Reappearance     of     nuclear    membrane     and     nucleolus;     two     complete 
daughter   cells,    each    containing   a   resting   nucleus.      (E.    B.    Wilson,    "The    Cell.") 


first  makes  its  appearance.  As  cell  division  proceeds,  two  layers 
of  cells  are  produced;  viz.,  the  ectoderm,  which  corresponds  to  the 
original  layer  of  the  blastodermic  vesicle,  and  the  entoderm,  or 
inner  layer.  Later  a  third  layer  appears  between  the  ectoderm 
and  the  entoderm,  called  the  mesoderm.  The  three  layers  together 
are  called  the  blastoderm. 

The  tissues  derived  from  these  layers  are  as  follows : 

Ectoderm. — Epithelium  of  the  skin  and  all  its  appendages,  as  hair,  nails 
enamel  of  teeth,  mammary,  sebaceous  and  sweat  glands,  includ- 
ing the  muscle  of  latter. 


ob  GENERAL    PATHOLOGY 

All  epithelium  not  mentioned  under  mesoderm  and  entoderm,  viz., 
the  epithelium  of  mouth  and  nose  with  their  glands  and  cavi- 
ties; of  membranous  labyrinth  of  car;  of  anus  and  of  that 
portion  of  male  urethra  anterior  to  the  prostate  gland. 

Entire  nervous  system,  with  the  retina,  crystalline  lens,  and  mus- 
cle of  the  iris. 

Mesoderm. — All  connective  tissue. 

All  muscle  tissue,  except  as  stated  under  ectoderm. 
All  lymphatic   tissue,  spleen,  bone-marrow  and  blood  cells. 
All  endothelium*   (of  vessels  and  serous  cavities). 
The  epithelium  of  the  genito-urinary  tract,  except  ureter,  Madder, 
female  urethra  and  prostatic  portion  of  male  urethra. 

Entoderm. — Epithelium   of   alimentary   tract     (except    mouth    and    anus)  ;     of 
Eustachian  tube  and  tympanum. 
Epithelium   of    respiratory    tract    (except   nose)  ;    also   of   thymus 
and  thyroid  glands. 

Epithelium  of  urt  tt  r,  bladdt  r,  f<  male  urt  thra  and  prostatic  portion 
of  male  un  thra. 


1The  endothelia  arc  included  among  the  epithelia  by  some  histologists;  others  again 
distinguish  between  the  "endothelium"'  of  blood  and  lymph  vessels,  and  the  ''mesothelium" 
ot  serous  cavities,  the  genito-urinary  epithelium  of  mesodermal  origin,  and  striated  and 
heart  muscle. 


CHAPTER  II 

THE  ETIOLOGY  OF  DISEASES 

While  therapeutics  is  the  art  of  healing  disease,  pathology  is 
the  science  of  investigating  disease,  and  this  investigation  is 
usually  pursued  under  the  following  headings : 

1.  Etiology,  or  investigation  of  the  causes  of  disease. 

2.  Morbid,  or  pathologic  anatomy,  the  changes  of  structure. 

3.  Morbid,  or  pathologic  chemistry,  the  changes  in  composi- 
tion. 

4.  Morbid,  or  pathologic  physiology,  the  changes  in  function. 
Of  these,  morbid  anatomy  has  been  the  most  highly  developed, 

and  forms  the  major  portion  of  the  text  in  most  works  on  pa- 
thology. 

Morbid  anatomy,  or  morphologic  pathology,  is  divided  into : 

(a)  Gross,  or  macroscopic  pathology,  dealing  with  the  gross 
or  naked-eye  appearances,  and 

(b)  Pathologic  histology,  or  microscopic  pathology,  dealing 
with  minute  or  microscopic  appearances. 

Etiology  of  Disease 

The  causes  of  disease  are  usually  divided  into  (a)  predispos- 
ing, indirect  or  mediate  causes,  and  (b)  specific,  direct,  imme- 
diate, exciting  or  determining  causes.  Predisposing  causes  in- 
clude all  conditions,  influences  and  agencies  which  increase  the 
individual's  susceptibility  to  disease,  while  the  specific  causes 
are  the  direct  and  final  factors  which  culminate  in  the  outbreak 
of  disease  and  determine  its  nature.  There  is  no  definite  divid- 
ing line  between  the  two  divisions;  predisposing  causes  may  at 
times  become  exciting  causes  and  vice  versa,  as  when  the  ex- 
posure to  extreme  cold  may  directly  cause  necrosis  or  inflamma- 
tion, while  a  prolonged  chilling  may  predispose  to  pneumonia, 
rheumatism,  etc.  In  the  main,  however,  predisposing  causes 
form  a  class  distinct  from  the  determining  causes,  and  in  the 
great  majority  of  instances,  the  body  as  a  whole,  or  the  part 

37 


38  GENERAL   PATHOLOGY 

or  parts  subsequently  affected,  are  first  acted  upon  by  the  pre- 
disposing causes,  preparing  the  tissues  for  the  successful  inva- 
sion or  development  of  the  real  specific  causative  factors. 

Predisposing  causes  may  be  such  biological  conditions  as  sex. 
age.  or  race:  or  the  predisposition  may  be  acquired  by  previous 
disease,  traumatism,  injurious  occupations,  unsanitary  surround- 
ings, bad  habits  of  life,  personal  vices,  etc.,  or  again,  such  pre- 
disposition may  be  hereditary. 

Some  of  the  principal  predisposing  causes  may  be  briefly  con- 
sidered: 

Age. — Children  are  especially  liable  to  gastrointestinal  disease 
because  of  the  delicacy  of  these  organs,  and  the  abundance  of 
lymphoid  structures ;  to  osteomyelitis,  because  of  the  vascularity 
of  the  growing  bones:  to  rickets,  a  nutritional  disease  involving 
principally  but  not  exclusively  the  bones  of  the  body:  to  diph- 
theria, whooping  cough,  measles,  chicken  pox.  scarlatina,  etc. 
Some  of  these  diseases,  particularly  measles,  are  very  contagious 
and  confer  life-long  immunity,  hence  their  prevalence  in  child- 
hood and  their  rare  occurrence  in  later  life. 

In  adolescence  certain  physical  and  mental  disorders  and 
anemic  conditions  are  apt  to  be  met  with. 

The  "prime  of  life,"  from  maturity  to  middle  age.  is  on  the 
whole  probably  the  period  most  free  from  disease,  still  at  this 
time  occur  those  diseases  which  depend  upon  free  association 
with  other  persons,  upon  exposure  to  inclement  weather  and  to 
occupational  hazards.  After  middle  age  incipient  degeneration 
of  the  vital  organs  and  tumors,  particularly  carcinomata.  appear, 
while  old  age  is  subject  to  more  pronounced  organic  changes  and 
sclerotic  conditions  of  the  vessels  and  the  trabecular  of  organs, 
predisposing  to  distinct  visceral  disease,  apoplexy,   etc. 

Sex. — Apart  from  the  diseases  peculiar  to  the  different  sexual 
organs  of  the  male  and  female,  men  as  a  rule  are  more  exposed 
to  adverse  climatic  conditions,  to  dangerous  pursuits,  hence  suf- 
fer from  diseases  liable  to  be  favored  by  these  predisposing  fac- 
tors. Men,  as  a  class,  are  also  inclined  to  a  far  greater  extent 
than  women  to  indulge  in  excesses  of  all  kinds,  and  are,  there- 
fore, more  subject  to  alcoholism,  gout,  and  venereal  disease,  and 
to  the  great  number  of  mental,  nervous,  and  visceral  pathologic 
changes  which  follow  such  diseases. 


ETIOLOGY    OF   DISEASES  30 

Race.  Sonic  races  are  more  susceptible  to  certain  diseases, 
especially  infectious  diseases,  than  are  others.  The  negro  is 
relatively  immune  to  yellow  fever  and  malaria,  probably  because 
his  tissues  produce  a  greater  number  of  antibodies  due  to  sub- 
infections  or  the  fact  that  his  race  has  been  exposed  to  such  dis- 
eases for  a  longer  time  and  to  a  greater  extent  than  the  white 
race.  On  t lie  other  hand,  the  negro  is  more  susceptible  to  tuber- 
culosis. The  American  Indian  and  the  Eskimo  are  free  from 
tuberculosis  in  the  native  surroundings  (lack  of  exposure?)  but 
succumb  readily  to  this  disease  when  brought  into  civilized  com- 
munities (due  largely  to  lack  of  resistance — antibodies).  The 
Japanese  are  said  to  be  comparatively  free  from  scarlet  fever,  the 
Chinese  from  cholera,  while  the  Hebrew  race  is  said  to  be  more 
susceptible  to  diabetes  than  other  races. 

Idiosyncrasy. — This  is  a  marked  susceptibility  which  certain  in- 
dividuals have  to  the  action  of  certain  drugs,  infections,  foods, 
and  even  odors.  The  smallest  doses  of  quinine  will  cause  ex- 
tensive and  painful  eruptions  in  some  persons;  the  pollen  of  cer- 
tain plants  will  result  in  coryza  and  hay  fever,  or  "pollen  dis- 
ease." Strawberries,  raspberries,  lobster,  and  many  foods  give 
rise  to  urticarial  eruptions  in  certain  individuals.  No  satisfac- 
tory explanation  of  this  individual  hypersensitivity  has  yet  been 
offered.  A  pronounced  excitability  of  the  nervous  system  may 
partly  explain  some  cases,  while  in  regard  to  idiosyncrasies  to- 
ward drugs  or  chemicals  it  has  been  assumed  that  the  cell  con- 
stituents of  the  individuals  affected  contain  atomic  groups  which 
readily  combine  with  the  substances. 

Traumatisms. — Injuries  of  all  kinds  act  by  causing  shock  and 
reducing  the  normal  vital  resistance.  A  fracture  of  the  shoulder 
or  other  part  of  the  body  framework  may  predispose  to  pneu- 
monia; extensive  burns  lead  to  degenerations  of  the  internal  or- 
gans, etc. 

Injurious  Occupations. — The  inhalation  of  noxious  gases  predis- 
poses to  respiratory  and  anemic  disease;  dust,  particularly  coal 
dust,  leads  to  fibroid  pneumonia  and  tuberculosis.  Painters  ab- 
sorb lead  and  suffer  from  intestinal  derangements  in  consequence. 
Occupations  requiring  mental  worry  or  prolonged  and  intense 
concentration  have  a  marked  depressing  effect  upon  the  general 
health. 


•40  GENERAL    PATHOLOGY 

Unsanitary  Surroundings. — It  must  be  self-evident  that  the 
health  of  individuals  who  dwell  or  work  in  buildings  that  are 
poorly  ventilated,  or  that  are  located  amid  unclean  or  filthy  sur- 
roundings, or  in  low,  poorly  drained  sections,  or  where  the  in- 
mates are  subjected  to  the  dust,  smoke  or  fumes  of  large  indus- 
tries, will  be  seriously  affected  and  predisposed  to  disease. 

Habits. — Intemperance,  whether  in  eating,  drinking,  use  of  to- 
bacco, use  of  drugs,  sexual  indulgence,  etc.,  drains  the  human 
economy  of  its  health  reserve  factors  and  makes  it  vulnerable  to 
disease.  Overwork  and  excessive  play  or  recreation,  in  fact,  ex- 
cess in  any  line  of  human  activity  should  also  be  included  in  the 
term  "intemperance."  A  proper  variation  of  work  and  play, 
of  mental  or  physical  exertion  and  rest,  is  the  only  rule  by  which 
the  normal  health  of  the  average  individual  may  be  conserved. 

Heredity. — Heredity  is  the  transmission  of  certain  characteris- 
tics or  tendencies  from  parent  to  offspring.  The  maternal  charac- 
teristics are  present  in  the  ovum,  and  the  paternal  in  the  sper- 
matozoon, the  essential  living  parts  of  these  parental  elements 
being  known  as  the  germ  plasm.  Heredity  therefore  refers  to  the 
qualities  contributed  by  either  parent  at  the  time  of  impregna- 
tion, and  has  nothing  to  do  with  conditions  which  may  affect  the 
health  or  development  of  the  fetus  during  its  life  in  utero.  Thus 
certain  diseases,  as  smallpox,  measles,  or  syphilis,  may  be  ac- 
quired by  the  mother  subsequent  to  impregnation,  and  may  be 
transmitted  to  the  fetus  through  the  placental  circulation.  The 
evidences  of  these  diseases  may  be  evident  when  the  child  is 
born,  but  they  are  not  hereditary,  but  congenital,  that  is,  dis- 
eases "acquired  in  prenatal  life."  It  is  usually  held,  however, 
that  certain  diseases,  particularly  syphilis,  may  also  be  trans- 
mitted through  the  germ  plasm  and,  therefore,  be  hereditary, 
but  as  a  rule  it  is  merely  the  tendency  to  disease ;  i.e.,  the  par- 
ticular impairment  of  health  which  favors  the  subsequent  devel- 
opment of  a  certain  disease,  that  is  inherited,  and  not  the  dis- 
ease itself  or  its  specific  cause.  As  an  example,  tuberculosis  may 
be  given,  for  it  is  generally  accepted  at  the  present  time  that  a 
lowered  resistance  or  predisposition  to  tuberculous  infection  may 
be  inherited,  but  not  the  tubercle  bacillus.  Diathesis  is  merely 
another  term  for  an  inherited  predisposition  to  disease ;  thus  we 
speak  of  hemorrhagic,  rheumatic  or  tuberculous  diatheses.     In 


ETIOLOGY    OF    DISEASES  41 

consanguineous  marriages  (marriages  of  blood  relatives)  the  off- 
spring may  suffer  from  an  accentuation  or  "accumulation"  of 
certain  family  weaknesses  or  diatheses. 

Tl  "will  be  seen  that  heredity  is  usually  a  predisposing  factor, 
and  only  in  ;i  few  instances  (and  these  no1  admitted  by  all  au- 
thorities) the  direel  cause  of  disease. 

Specific  or  Determining  Causes. — These  may  be  physical  or 
chemical  agencies,  living  organisms  or  autointoxication. 

Traumatism. — Mechanical  injuries,  as  blows,  falls,  knife  or  gun- 
shot wounds,  etc.,  result  in  concussion,  contusion,  abrasion,  lac- 
eration or  rupture  of  the  soft  tissues,  or  fracture  of  the  bony 
tissues.  Tn  all,  except  concussion,  there  occurs  a  certain  amount 
of  hemorrhage,  which  may  be  interstitial,  as  in  contusions,  or 
external,  or  into  natural  body  cavities.  Disintegration  of  the 
blood  and  injured  tissues  results  with  more  or  less  inflammation. 

Concussion  is  the  violent  jarring  of  an  organ,  accompanied 
by  slight,  profound,  or  fatal  shock,  but  unaccompanied  by  visible 
changes  in  the  structure  of  the  organ.  In  concussion  of  the  brain, 
the  vital  centers  are  excessively  stimulated  by  the  blow,  then 
depressed,  or  in  fatal  cases,  paralyzed.  Contusion  (or  bruising) 
and  laceration  may  be,  and  often  are,  associated  with  concus- 
sion, but  are  not  essential  features  of  the  latter. 

SJiock  is  a  depression  of  the  vital  centers,  particularly  the  car- 
diac and  respiratory  centers,  resulting  in  weakened  heart  action, 
irregular  breathing,  lowering  of  the  bodily  temperature,  pallor, 
and  clamminess  of  the  skin.  Shock  may  be  caused  by  an  injury, 
or  by  a  strong  emotion,  as  great  fear,  acting  upon  the  nerve 
centers. 

Pressure  upon  a  part,  if  continuous,  will  result  in  atrophy.  In- 
termittent pressure  will  cause  atrophy  of  some  of  the  constituents 
of  the  tissues  affected,  and  hyperplasia  of  others,  particularly  the 
connective  tissues. 

Heat. — A  moderate  excess  of  heat,  locally  applied,  will  cause 
hyperemia;  a  higher  degree  will  cause,  in  addition,  necrosis,  par- 
ticularly vesication  (liquefaction  necrosis).  A  still  higher  de- 
gree of  heat  will  char  or  burn  the  tissues,  with  oxidation  of  the 
superficial  parts  and  necrosis  of  the  deeper  parts.  Burns  which 
cover  one-third  of  the  surface  of  the  body  are  nearly  always 
fatal,  due  to  absorption  of  toxic  products  formed  in  the  burned 


42  GENERAL    PATHOLOGY 

tissues,  and  to  the  fact  that  a  large  part  of  the  eliminating  sur- 
face of  the  skin  is  destroyed.  In  severe  cases  death  is  due  to 
shock. 

First  degree  burns  are  those  that  are  characterized  by  swelling 
and  reddening  of  the  skin;  second  degree  burns,  by  the  forma- 
tion of  vesicles  (or  blisters)  and  bulla?;  third  degree  burns,  by 
destruction  of  all  the  layers  of  the  integument  with  more  or  less 
of  the  subcutaneous  tissue  and  ulceration.  The  burns  so  de- 
scribed refer  only  to  burns  of  the  skin. 

Burns  may  proceed  deeply  into  the  tissues  (sometimes  called 
fourth  degree  burns)  with  coagulation  of  the  cells  and  other 
forms  of  necrosis  and  oxidation,  until  in  fact  the  whole  body  is 
incinerated  (completely  oxidized). 

Sunstroke  may  be  caused  by  exposure  to  the  heat  of  the  sun. 
The  bulbar  heat  centers  are  depressed  or  paralyzed  by  the  heat, 
or  metabolic  poisons  are  formed  by  the  heat  which  act  upon  the 
centers,  resulting  in  very  high  temperatures  (107°  to  112°)  with 
labored  breathing,  headache,  vertigo,  nausea,  delirium  and  finally 
coma. 

Heat  exhaustion  results  from  high  temperature  with  humidity, 
or  less  often  from  exposure  to  the  sun  alone.  This  is  probably 
due  to  vasomotor  paralysis,  and  the  symptoms  are  those  of  col- 
lapse with  subnormal  temperature ;  rapid,  weak  pulse ;  rapid, 
shallow  breathing;  and  livid  color. 

Cold. — The  primary  effect  of  cold  to  the  surface  is  contraction 
of  the  superficial  capillaries  causing  the  parts  to  appear  blanched 
and  anemic.  Soon  the  vasoconstrictors  are  paralyzed,  the  ves- 
sels dilate,  and  the  parts  become  swollen  and  livid  and  more  or 
less  painful  {frostbite).  In  a  severe  frostbite  the  part  becomes 
covered  with  vesicles,  the  blood  plasma  coagulates  with  disinte- 
gration of  the  blood  cells  and  thrombosis  of  the  vessels ;  gangrene 
may  or  may  not  follow.  Unless  gangrene  sets  in,  recovery  takes 
place,  but  in  many  cases  chilblain,  or  pernio  develops  as  a  secon- 
dary effect  of  frostbite.  This  is  a  condition  in  which  swelling 
and  pain  or  tingling  sensations  return  in  a  previously  frostbitten 
part  upon  approaching  a  fire,  upon  exercising,  or  exposure  to 
slight  cold.     Kepeated  attacks  lead  to  vesication  and  ulceration. 

Excessive  cold  will  coagulate  the  cells  and  fluids  of  a  part, 
with  subsequent  gangrene.     Sudden  exposure  to  very  low  tern- 


ETIOLOGY   OF    DISEASES  43 

peratures  produces  lesions  practically  identical  with  those  caused 
by  burns. 

Atmospheric  Pressure. — Increased  atmospheric  pressure  causes 
the  tissues  and  fluids  to  hold  more  gases  (almost  exclusively 
nitrogen),  and  subsequently  when  the  return  to  normal  pressure 
is  too  sudden,  bubbles  of  gas  appear  in  the  tissues  and  blood  ves- 
sels. At  first  these  bubbles  are  located,  only  in  the  capillaries, 
which  may  rupture  with  interstitial  hemorrhage,  bleeding  from 
mucous  surfaces,  as  nose,  accompanied  by  symptoms  of  nausea, 
palpitation  of  the  heart,  prostration,  delirium  and  palsies.  The 
tiny  bubbles  may  coalesce  into  larger  ones  and  form  air  emboli, 
or  gas  emboli,  which  are  apt  to  be  fatal.  At  necropsy  congestion 
of  the  central  nervous  system  and  thoracic  organs  have  been 
found,  with  hemorrhages  into  the  meninges  and  vacuolization  of 
the  spinal  cord.     This  condition  is  called  caisson  disease. 

Decreased  atmospheric  pressure  causes  vascular  and  nervous 
disturbances,  with  apparent  increase  of  the  red  blood  cells  and 
hemoglobin  due  to  the  escape  of  the  plasma  into  the  tissues  (rel- 
ative polycythemia).  The  symptoms  may  be  due  to  lack  of 
oxygen,  together  with  the  mechanical  effect  of  decreased  pres- 
sure upon  the  tissues.  This  condition  is  sometimes  called  moun- 
tain disease. 

Electricity. — Powerful  electrical  currents  usually  kill  by  pa- 
ralysis of  the  heart.  The  local  effects  may  be  demonstrable  or 
not,  according  to  the  nature  of  the  conductors  and  the  parts 
affected,  as  well  as  the  intensity  and  duration  of  the  current. 
Frequently  there  are  burns,  which  may  be  deep  and  dry;  the 
brain  and  meninges  are  congested,  and  there  may  be  minute 
hemorrhages  into  the  gray  matter,  floor  of  the  fourth  ventricle, 
and  other  parts,  with  congestion  of  the  thoracic  and  abdominal 
organs.  Lightning  strokes  often  cause  peculiar  branching  linear 
burns  upon  the  skin ;  and  the  clothing,  and  particularly  the  foot 
Avear,  may  be  torn  into  shreds,  and  even  internal  organs  have 
been  found  to  be  lacerated. 

Light. — Light  is  usually  regarded  as  beneficial  to  the  health 
of  the  higher  organisms,  but  it  is  harmful  to  unicellular  organ- 
isms, as  bacteria;  in  fact  sunlight  is  bactericidal.  Strong  sun- 
light may  cause  hyperemia  or  inflammation  of  the  skin  (sunburn), 


44  GENERAL   PATHOLOGY 

which,  if  severe,  may  proceed  to  vesication  and  ulceration.  In- 
tense light  of  any  kind,  as  calcium  light,  may  cause  retinitis. 

X-rays. — X-rays  cause  degenerative  changes  in  the  cells,  and 
finally  disintegration.  The  cells  of  diseased  tissues  are  more 
easily  destroyed  than  healthy  cells.  Chronic  dermatitis  with  a 
tendency  to  epitheliomatous  change  is  apt  to  follow  x-ray  burns 
of  the  skin.  Highly  specialized  cells,  as  spermatozoa,  are  readily 
destroyed  by  exposure  to  these  rays. 

Chemical  Agents. — Any  substance  which  by  its  chemical  ac- 
tion destroys  (corrodes)  tissues,  or  which,  when  absorbed  and 
carried  to  various  cells,  causes  harm,  is  called  a  poison.  A  sub- 
stance may  be  a  therapeutic  agent  as  well  as  a  poison,  depending 
upon  the  amount  introduced  into  the  tissues.  One-fortieth  of  a 
grain  of  arsenic  is  a  stimulant  to  the  nervous  system  and  the 
hematopoietic  organs,  and  therefore  a  useful  tonic,  but  one  or 
two  grains  will  cause  death. 

The  study  of  poisons  is  too  extensive  a  subject  to  be  under- 
taken, even  in  a  summary  manner,  in  a  work  of  this  kind,  and 
the  reader  is  referred  to  works  on  toxicology  for  their  further 
consideration. 

Living  Organisms. — Living  organisms  are  the  most  important 
direct  causes  of  disease,  and  will  be  considered  in  Chapter  VIII. 

Autointoxication,  or  self-poisoning,  is  a  diseased  condition 
caused  by  the  accumulation  in  the  tissues  of  an  abnormal  amount 
of  normal  waste  products,  as  a  result  of  impaired  elimination, 
or  by  the  formation  of  abnormal,  toxic  substances,  as  a  re- 
sult of  impaired  metabolism,  or  impaired  gastrointestinal  di- 
gestion. Poisoning  due  to  the  mere  absorption  of  products  of 
intestinal  putrefaction  is  not  included  in  this  term. 


CHAPTER  III 

PATHOLOGIC  PROCESSES 

All  pathologic  processes  are  either  (1)  simple — those  in  which 
the  changes  are  of  one  kind  only,  as  in  atrophy,  or  (2)  compound 
— those  in  which  two  or  more  simple  processes  are  taking-  place 
at  the  same  time,  as  in  inflammation. 

Pathologic  pi'oeesses  may  also  be  divided  into  (a)  progressive, 
in  which  tissues  are  built  up,  and  (b)  retrograde  or  retrogressive, 
in  which  tissues  are  broken  down. 

RETROGRADE  PROCESSES 
Atrophy 

Atrophy  is  a  simple  retrograde  process,  resulting  in  the  de- 
crease in  size  of  a  part  or  an  organ.  Normal  examples  are  the 
atrophy  of  the  thymus  gland  after  the  first  few  years  of  child- 
hood, of  the  uterus  after  parturition,  of  the  overies  after  the 
menopause. 

Atrophy  may  be  divided  into  simple  atrophy,  which  is  a  de- 
crease in  the  size  of  the  cells,  and  numerical  atrophy,  a  decrease 
in  the  number  of  the  cells.  More  often  these  two  types  are  as- 
sociated or  combined,  hence  sometimes  called  combined  atrophy. 
Simple  atrophy  when  unaccompanied  by  any  other  pathologic  proc- 
ess is  a  true  atrophy,  while  numerical  atrophy,  in  which  the  cells 
are  usually  first  degenerated  (hence  degenerative  atrophy),  is  usu- 
ally accompanied  by  a  replacement  of  the  destroyed  cells  by 
fatty  tissue  or  a  hyperplasia  of  connective  tissue,  making  it  ex- 
tremely difficult  to  distinguish  between  atrophy  and  degenera- 
tion with  replacement. 

The  term  "atrophy"  usually  refers  to  local  atrophy  (affecting 
one  or  more  parts)  while  atrophy  of  all,  or  nearly  all  parts  of  the 
body  (emaciation)  is  sometimes  called  general  atrophy.  Hypopla- 
sia, infantilism,  nanism,  ateleiosis,  etc.,  are  terms  referring  to  va- 
rious forms  of  underdevelopment  or  stunted  growth,  and  must  not 

45 


46 


GENERAL    PATHOLOGY 


be  confounded  with  atrophy.    Aplasia  or  agt  nesia  moans  total  lack 
of  development  of  a  part. 

Etiology. — The  causation  of  normal  atrophy  is  not  well  under- 
stood, but  pathologic  atrophy  is  due  to  diminished  nutrition  of  a 
part,  depending  upon : 

1.  Prolonged,  continuous  pressure  ("pressure  atrophy,"  as  by 
tumors,  aneurysms,  corsets,  etc). 

2.  Disuse,  as  in  fractures,  paralysis,  habit,  etc. 

3.  Loss  of  trophic  influence,  as,  in  muscular  atrophy  due  to 
disease  of  the  spinal  cord  (neuropathic  atrophy). 

4.  Starvation,  general  or  local,  as  from  obstructed  blood  vessels. 

5.  Senility,  affecting  especially  the  heart,  lungs,  liver,  kidneys, 
testicles,  uterus  and  bones. 

Locations. — Any  part  of  the  body  may  become  atrophied. 


■\      I        I. 

f-fj  | 

r    /   :  I 


* 


Fig.   3. — Brown  atrophy  of  the  heart  muscle.      (Stengel  and  Fox.) 


Gross  Morbid  Anatomy. — In  true  atrophy,  the  part  or  organ 
is  diminished  in  size  without  change  in  shape  or  consistence.  In 
the  degenerative  type,  the  shape  is  usually  much  altered,  the 
size  unaltered  or  decreased,  and  the  consistence  increased,  or  de- 
creased according  to  the  nature  of  the  tissue  which  has  re- 
placed the  atrophied  cells.  In  both  forms  the  color  is  usually 
increased,  becoming  darker,  from  a  relative  or  absolute  increase 
of  pigment. 

Pathologic  Histology. — In  true  atrophy  the  cells  are  smaller 
than  normal,  and  pigment  granules  can  usually  be  seen.  In 
brown  atrophy  of  the  heart,  these  granules  are  arranged  about 
the  poles  of  the  more  or  less  elongated  nucleus  (Fig.  3).  In 
numerical  atrophy,  the  parenchymatous  cells  are  smaller,  fewer 
in  number,  and  in  places  altogether  absent,  and  in  their  stead 


PATHOLOGIC    PROC1 


47 


may  be  seen  connective-tissue  elements,  hyaline,  Eatty  or  mucoid 
material,  and  some  type  of  pigmentation. 

Pathologic  Physiology. — Since  the  parenchyma  of  organs  is 
chiefly  though  no1  exclusively  affected,  function  is  always  im- 
paired— secretion  diminished,  muscular  activity  lessened,  etc. 

Results. — If  the  process  is  arrested  early,  partial  or  complete 
restoration  may  be  attained;  if  not,  death  of  the  part  will  result 
with  iis  disappearance  and  replacement  by  other  tissue. 


Degenerations  (or  Metamorphoses) 

Degenerations  are  simple  retrograde  processes  in  which  the 
cells  or  the  intercellular  substances  are  converted  into  a  ma- 
terial abnormal  in  kind  or  quantity. 


Fig.    4. — Albuminous    degeneration — kidney.       (Delafield    and    Prudden.) 

There  are  six  types  of  degeneration: 

Cloudy  swelling,  or  parenchymatous  or  albuminous  degenera- 
tion. 

Fatty  degeneration. 

Mucoid  or  myxomatous  degeneration. 

Colloid  degeneration. 

Hyaline  degeneration. 

Amyloid  degeneration.  "Whether  amyloid  is  an  infiltration  or 
a  degeneration  can  not  be  definitely  stated — even  its  chemical 
composition  is  not  yet  definitely  determined  (see  Etiology  of 
Amyloid  Degeneration). 


48  GENERAL   PATHOLOGY 

Cloudy  Swelling-,  Parenchymatous  or  Granular  Degeneration 

Cloudy  swelling  is  a  simple  retrograde  process  in  which  the 
soluble  albuminous  elements  of  the  cells  are  precipitated  as  in- 
soluble granules,  associated  with  an  increase  of  fluids  in  the  cells. 
(Fig.  4.) 

Etiology. — Cloudy  swelling  is  caused  by  the  action  of  poisons, 
as  (a)  toxins  of  infectious  diseases,  particularly  scarlet  fever, 
diphtheria,  and  typhoid  fever,  (b)  extraneous  poisons,  as  ether, 
chloroform,  mercury,  etc.;  and  (c)  poisons  formed  within  the 
body,  as  in  autointoxication,  the  metabolic  disturbances  accom- 
panying high  temperature  (pyrexia),  absorption  of  necrotic  tis- 
sue or  disintegrating  materials,  etc. 

Locations. — Chiefly  the  parenchyma  of  organs,  particularly 
renal  epithelium,  mucous  membranes,  liver  cells,  voluntary  mus- 
cle and  heart. 

Gross  Morbid  Anatomy. — The  organ  is  uniformly  enlarged, 
owing  to  the  swollen  conditions  of  the  cells ;  paler  than  normal, 
due  to  the  whiteness  of  the  granules  and  the  anemia  caused  by 
the  pressure  of  the  swollen  cells;. softer,  owing  to  the  increased 
fluid  content.  On  section  the  surface  is  moist  and  the  parenchyma 
protrudes. 

Pathologic  Histology. — The  cell  is  full  of  fine  granules,  which 
partly  or  wholly  obscure  the  nucleus  and  the  striations  of  muscle 
fibers.  The  cells  are  increased  in  size  and  more  or  less  irregular 
in  outline.  The  cell  vail  is  sometimes  indistinct,  causing  the  cells 
to  have  the  appearance  of  having  coalesced. 

Reactions. — The  granules  may  be  dissolved  in  acetic  acid,  thus 
causing  the  reappearance  of  the  nuclei,  but  they  are  insoluble  in 
alcohol  or  ether,  thus  differentiating  them  from  fat  globules  or 
granules. 

Pathologic  Physiology. — Function  is  impaired  due  to  the  pres- 
ence of  the  granules  and  the  intracellular  fluids. 

Results. — Granular  degeneration  is  a  temporary  condition  oc- 
curring in  acute  disease,  and  complete  recovery  is  the  rule,  but  if 
the  causes  persist,  fatty  or  other  degeneration  ensues. 

Fatty  Degeneration 

Fatty  degeneration  is  a  simple  retrogressive  process  in  which 
there  is  disintegration  of  the  cellular  protoplasm,  with  appearance 


PATHOLOGIC    PROCESSES  I'l 

of  fat  within  the  cell.  Normal  examples  are  the  production  of 
t'al  globules  in  the  secretion  of  milk,  and  the  change  of  red 
(fetal)  ft)  yellow  (adult)  bone  marrow.     (Fig.  5.) 

Etiology.  Since  cloudy  swelling  may  pass  into  Tally  degenera- 
tion, the  prolonged  action  of  toxins  and  poisons  which  cause  the 
former  will  also  cause  the  latter.  Patty  degeneration  also  oc- 
curs in  pernicious  anemia  and  in  cachexias,  due  to  some  form  of 
toxin;  and  in  the  involution  of  tissues,  as  thymus,  corpora  lutea, 
uterus,  etc. 

Locations. — Fatty  degeneration  occurs  in  the  parenchyma  of 
organs,  and  at  times  also  in  the  connective  tissues,  as  in  athero- 
matous vessels. 

Gross  Morbid  Anatomy. — The  organ  is  smaller  (though  in  early 


Fig.    5. — Fatty    defeneration — kidney.       (Delalield    and    Prudden.) 

stages  it  may  be  enlarged)  and  softer  than  normal.  The  color 
is  pale  yellow,  due  to  the  presence  of  fat,  but  congestion,  pigmen- 
tation, or  jaundice  may  alter  the  color.  The  specific  gravity  is 
reduced.  The  area  affected  may  be  uniform  or  the  degeneration 
appear  in  streaks,  as  in  the  heart  and  liver,  thus  producing  a 
mottled  appearance.     On  section  the  knife  becomes  greasy. 

Pathologic  Histology. — The  cells  are  in  the  early  stages  usually 
somewhat  larger  than  normal,  but  later  are  shrunken,  irregular 
in  shape,  and  more  or  less  degenerated  as  shown  by  their  di- 
minished staining  qualities.  The  cells  are  partly  or  in  later 
stages  completely  filled  with  small,  discrete,  highly  refractile 
fatty  granules,  scattered  irregularly  throughout  the  cytoplasm. 
In  acute  or  very  advanced  cases  these  fat  granules  may  coalesce 
into  globules,  which  in  exceptional  cases  may  become  quite  large. 


50  GENERAL    PATHOLOGY 

At  first  the  nucleus  is  not  affected,  but  in  late  stages  of  the  dis- 
ease it  shows  degenerative  changes  (karyolysis).  Cells  crowded 
with  fat  granules  are  sometimes  called  "compound  granule 
cells." 

Pathologic  Chemistry. — In  fatty  degeneration,  the  cells  are  first 
degenerated  by  the  poisons  indicated  in  describing  its  etiology, 
followed  in  the  main  by  an  infiltration  of  fat  from  without.  In 
the  kidneys,  spleen,  and  muscles,1  however,  the  fat  is  formed 
principally  by  the  setting  free  of  the  intracellular  fat  from  its 
combination  with  the  protein  substances  by  autolysis,  i.e.,  the  fat 
previously  present  but  invisible  is  rendered  visible. 

Reactions. — Fat  is  soluble  in  alcohol,  ether,  and  chloroform; 
but  is  not  dissolved  by  acetic  acid.  It  is  stained  red  by  Scharlach 
E,  and  orange  by  Sudan  in.  Osmic  acid  stains  fat  a  deep  black, 
due  to  the  olein  present  in  all  natural  fats. 

Pathologic  Physiology. — Impairment  and  finally  destruction  of 
the  secreting  or  muscular  functions  (as  in  heart  muscle)  result, 
In  the  liver  and  kidney  secretion,  however,  is  well  maintained 
even  in  advanced  cases. 

Results. — Mild  cases  with  uninvolved  nuclei  may  recover,  but 
the  condition  is  generally  irremediable,  the  degeneration  pro- 
ceeding to  complete  death  of  the  cells  (necrobiosis)  with  depo- 
sition of  fatty  acid  crystals,  cholesterin,  etc.,  or  the  damaged  tis- 
sue may  undergo  calcification. 

Mucoid  Degeneration 

Mucoid  degeneration  is  a  simple  retrogressive  process  in  which 
there  is  a  conversion  of  the  cells  or  intercellular  substance  into 
some  type  of  mucin.  Normal  examples  are  the  secretions  of  the 
goblet  cell  of  the  mucous  membrane,  and  Wharton's  jelly  of  the 
umbilical  cord.     (Fig.  6.) 

Etiology. — The  causes  which  bring  about  this  form  of  de- 
generation are  not  definitely  known.  Inflammation  is  a  factor 
when  mucoid  degeneration  appears  in  mucous  membranes. 

Locations. — (a)  Mucous  membrane,  affecting  the  columnar  cells, 
resulting  in  the  formation  of  a  large  number  of  goblet  cells,  (b) 
Intercellular  substance  of  subcutaneous,  subserous  and  submucous 


'Wells,    II.    Gideon,    Chemical    Pathology,    Philadelphia,    W.    B.    Saunders    Co. 


PATHOLOGIC    PROC]  SSES 


51 


tissues,  either  as  a  diffuse  process  (myxedema),  or  as  a  local 
process  in  nasal  polyps,  hydat  il'orm  moles,  etc.  (c)  In  tumors,  as 
ovarian  cysts,  carcinoma  springing  from  mucous  membranes  (the 
so-called  "colloid  cancers"),  myxomata,  etc. 

Gross  Morbid  Anatomy. — The  mucous  membranes  are  covered 
with  a  viscid  semigelatinous  and  colorless  material,  while  in  the 
antrum  of  Highmore,  salivary  glands,  etc.,  there  are  cyst-like  col- 
lections of  the  same  material.  When  affecting  the  connective 
tissues,  these  are  soft,  elastic  and  tear  easily.  In  tumors  the 
mucoid  material  is  drier;  in  ovarian  cysts  the  material  may  as- 
sume large  proportions. 


. > 

Fig.   6. — Mucoid   degeneration   of  fibrous  tissue.      (Delafield  and   Prudden.) 


Minute  Morbid  Anatomy. — The  cells  are  partly  or  completely 
filled  with  the  mucus:  the  typical  "goblet  cells"  are  distended 
and  the  nucleus  pressed  to  one  side.  The  material  is  usually 
homogeneous,  but  in  connective  tissues  it  may  appear  as  granules 
or  as  coarse  shreds  lying  between  the  cells;  the  cells  present  all 
stages  of  degeneration  from  the  normal  appearance  to  typical 
mucoid  cells,  with  irregularly  stellate  outline. 

Pathologic  Chemistry. — Mucin  is  a  compound  protein  (gluco- 
samine normally  secreted  by  the  epithelium  of  mucous  mem- 
branes, and  also  occurring  in  the  mucoid  tissue  of  the  fetus, 
where  it  is  the  precursor  of  the  adult  connective  tissue.  The 
mucoid  degeneration  associated  with  inflammation  of  mucous 
membranes  (catarrhal  inflammation)   is  in  reality  only  a  path- 


52  GENERAL    PATHOLOGY 

ologic  increase  of  mucinous  secretion  of  epithelial  cells,  which  is 
essentially  true  also  of  this  substance  in  "colloid  cancers"  and 
ovarian  cysts;  the  pathologic  connective-tissue  mucin  is  merely 
a  reversion  to  the  fetal  type  of  connective  tissue.  In  ovarian 
cysts  this  product  differs  somewhat  in  chemical  properties  from 
true  mucin,  hence  called  pseudomucin. 

Reactions. — Mucin  swells  in  water,  dissolves  in  alkalies,  is  in- 
soluble in  acids  and  alcohol,  and  is  precipitated  by  acetic  acid. 
It  is  acid  in  reaction,  hence  takes  the  basic  stains.  Pseudomucin 
is  not  precipitated  by  acetic  acid,  is  alkaline  in  reaction,  and 
takes  the  acid  stains. 

Pathologic  Physiology.— Function  is  moderately  impaired  in 
mucous  membranes,  resulting  in  catarrhal  conditions.  In  connec- 
tive tissues,  the  change  is  apt  to  be  permanent  but  usually  causes 
no  serious  harm. 

Colloid  Degeneration 

This  is  a  simple  retrograde  pathologic  process  in  which  there 
is  a  conversion  of  the  cell  into  a  yellowish  brown  transparent  ma- 
terial, resembling  in  physical  appearance  the  colloid  material  of 
the  thyroid  gland.  (Fig.  7.) 

Pathologic  Chemistry. — The  colloid  of  the  thyroid  is  an  iodin- 
containing  globulin,  but  the  term  as  used  in  "colloid  degenera- 
tion" is  not  chemically  definite,  but  includes  such  substances  as 
have  a  colloid  appearance  (just  described).  "Colloid  cancer" 
was  so  named  because  the  mucoid  material  found  within  it  had 
a  colloid  appearance,  due  to  its  compression  within  a  confined 
space,  and  to  its  partial  loss  of  water.  Apart  from  that  found  in 
the  thyroid,  colloid  resembles  the  mucins  in  chemical  composi- 
tion, particularly  pseudomucin. 

Etiology. — The  etiology  is  obscure.  Pathologically  it  is  partly 
a  secretion  and  partly  a  degeneration  of  the  epithelial  cell. 

Locations. — It  occurs  in  goiters  and  other  tumors  of  the  thyroid 
gland,  in  the  hypophysis  cerebri,  kidneys,  adrenals,  prostate 
gland,  and  seminal  vesicles,  and  many  other  locations. 

Gross  Morbid  Anatomy. — The  organs  affected  may  be  larger, 
and  either  harder  or  softer  than  normal.  The  colloid  substance 
occurs  in  cystic  collections,  having  a  yellowish  brown  transparent 


PATHOLOGIC    PROCESSES  53 

appearance,  varying  in  size  from  minute  bodies  to  large  masses, 
having  the  consistence  of  calf's  fool  jelly.  A  serious  transuda- 
tion may  dissolve  the  colloid.  Leaving  cavities  Idled  with  choco- 
late-colored fluid. 

Pathologic  Histology. — The  material  firsl  appears  in  the  epi- 
thelial cells  as  droplets;  the  latter  become  completely  trans- 
formed into  colloid,  and  as  new  layers  of  cells  are  formed  and 
successively  degenerated,  the  acini,  tubules  or  cystic  cavities 
formed  to  receive  the  material,  become  distended  to  various  de- 
grees. The  substance  is  usually  homogeneous  in  appearance,  but 
may  show  concentric  lines  corresponding  to  the  layers  of  cells 
which  have  undergone  the  change. 


F'g-    7. — Colloid    degeneration    of   the    thyroid    gland   showing   masses    of   colloid    matter    in 
the   gland   acini.      (Karl    and    Schmorl.) 

Reactions. — Colloid  does  not  swell  in  water;  is  not  precipitated 
by  acetic  acid,  but  is  precipitated  by  tannic  acid.  Like  pseudo- 
mucin,  it  elects  the  acid  dyes,  but  the  more  nearly  it  approaches 
the  mucins  in  composition,  the  more  variable  are  its  staining 
properties. 

Pathologic  Physiology. — Function  is  impaired,  probably  on  ac- 
count of  the  pressure  to  which  1  lie  vital  elements  are  subjected 
by  the  material. 

Results. — Absorption  with  regeneration  of  epithelial  cells  is 
possible  in  some  cases.    When  the  process  has  caused  destruction 


54  GENERAL    PATHOLOGY 

of  considerable  amounts  of  parenchymatous  cells,  colloid  de- 
generation is  usually  followed  by  hyaline  mucoid,  necrotic  or 
calcareous  change. 

Hyaline  Degeneration 

Hyaline  degeneration  is  a  simple  retrograde  morbid  process 
with  the  appearance  in  the  cells  and  intercellular  substance  of  a 
homogeneous,  glistening,  opaque,  albuminous  material,  called 
hyaline  (glass-like).  (Fig.  8.) 

Pathologic  Chemistry. — This  material  is  closely  related  to  col- 
loid and  amyloid  substances,  being  distinguished  mainly  by  its 


Fig.    8. — Hyaline    degeneration    of    an    ovarian    capillary.       Oc.    2;    ob.    9.       (McFarland.) 

physical  properties  and  its  distribution.  Hyaline  is  not  a  chemical 
entity,  but  includes  a  number  of  different  chemical  substances, 
i.e.,  various  forms  of  degeneration  or  necrosis. 

Etiology. — The  causal  factors  are  not  well  understood.  Ar- 
teriosclerosis, and  all  forms  of  arteritis  favor  its  production ;  also 
the  toxins  of  infections  (chiefly  the  acute  infections,  as  scarlet 
fever)  and  septic  processes,  lead  poisoning,  etc.,  but  chronic  in- 
fectious disease,  as  tuberculosis,  syphilis,  etc.,  may  also  be  fol- 
lowed by  this  change. 

Locations. — It  may  be  found  in  any  part  of  the  body,  but  there 
are  three  principal  types:     (a)   Connective-tissue  hyaline,  found 


PATHOLOGIC    PROCESSES  55 

iii  dense  tissues,  as  old  scars,  sclerotic  vessel  walls,  capsules  and 
trabeculae  of  organs,  especially  of  the  spleen,  liver,  heart,  brain, 
cord,  etc. 

Von  Recklinghausen's  hyaline  is  thai  which  involves  the  cap- 
sules and  trabeculae  of  lymph  nodes,  especially  when  the  seat  of 
tuberculosis. 

(b)  Cellular  hyaline,  occurring  as  round  bodies  within  cells, 
such  as  epithelium  of  mucous  membranes  and  the  kidneys.  Zen- 
ker's hyaline  occurs  in  voluntary  muscle  cells,  as  the  rectus  ab- 
dominis, diaphragm  and  adductors  of  the  thigh  in  typhoid  fever, 
though  some  believe  this  to  be  amyloid  degeneration,  others,  a 
form  of  coagulation  necrosis. 

(c)  Necrotic  hyaline,  found  in  old  blood  clots  (hyaline 
thrombi),  in  fibrinous  and  inflammatory  exudates  (exudative  hy- 
aline), and  in  necrotic  tumors,  tubercles,  gummata,  etc. 

Russell's  "fuelisin  bodies"  are  small  round  hyaline  bodies,  con- 
centrically striated,  found  within  and  between  cells  of  epithelial 
tumors,  and  sometimes  in  normal  tissues.  Their  true  nature  is 
not  known,  but  they  resemble  hyaline  material  in  appearance  and 
in  affinity  for  acid  fuchsin  stains. 

Gross  Morbid  Anatomy. — Hyaline  is  not  usually  sufficiently 
abundant  to  be  seen  by  the  naked  eye,  but  when  so,  it  appears 
similar  to  hyaline  cartilage,  is  smooth,  and  cuts  with  the  same  re- 
sistance. In  mucous  and  serous  membranes,  small  collections 
may  appear  as  opaque  irregular  plates. 

Pathologic  Histology. — (a)  In  the  blood  vessels  hyaline  is  seen 
in  and  beneath  the  endothelium  as  a  homogeneous  material,  also 
between  the  vascular  coats,  or  around  the  vessels  (such  perivas- 
cular hyaline  is  especially  well  seen  in  cylindromata).  The  ves- 
sel wall  is  thickened,  the  lumen  narrowed,  and  possibly  ob- 
literated, (b)  In  interstitial  tissues,  hyaline  material  is  found 
between  the  muscle  fibers,  hepatic  cells,  renal  tubules  in  the 
reticulum  of  lymph  glands,  in  the  retina,  in  cicatrices,  and  in 
neoplasms,  (c)  Within  cells,  hyaline  material  occurs  as  homo- 
geneous bodies  in  muscle  cells,  giant  cells,  epithelium,  and  to  a 
lesser  extent  in  leucocytes  and  wandering  cells. 

Reactions. — Hyaline  is  resistant  to  reagents,  being  unaffected 
by  acids,  alkalies,  and  alcohol.  The  staining  reactions  are  varia- 
ble, owing  to  its  variable  composition,  but  usually  hyaline  ma- 


56  GENERAL   PATHOLOGY 

ferial  has  a  decided  affinity  for  acid  fuehsin.  and  other  acid 
stains ;  but  the  older  the  hyaline,  the  paler  it  stains.  Thionin 
stains  it  red  and  other  tissues  bine. 

Pathologic  Physiology. — Hyaline  degeneration  does  not  impair 
function  as  a  rule:  but  if  it  is  extensive,  it  may  affect  the  paren- 
chyma by  compression  or  by  anemia  through  narrowed  blood  ves- 
sels. 

Results. — It  may  be  absorbed,  or  converted  into  fatty  degenera- 
tion, or  undergo  caseation  or  calcification. 

Amyloid  Degeneration  (Waxy,  Bacony,  or  Lardaceous 
Degeneration) 

Amyloid  degeneration  is  a  simple  retrograde  process  with  the 
appearance  in  the  intercellular  substance  of  connective  tissues  of 
a  waxy  albuminous  material,  called  amyloid.     (Fig.  9.) 


Fig  9. — Amyloid  infiltration  of  capillary  walls   in  kidney  glomerulus.      (Stengel   and  Vox.) 

Pathologic  Chemistry. — This  substance  was  at  first  thought  to 
be  a  form  of  cellulose  because  it  gave  the  blue  color  with  iodine 
when  followed  by  sulphuric  acid,  and  was  hence  called  "amy- 
loid" or  starchlike,  but  is  now  believed  to  be  a  protein  combined 
with  chondroitin-sulphuric  acid:  though  Hansenn  failed  to  find 
any  of  the  latter  in  amyloid  of  the  spleen,  thus  making  the  cheni- 
istrv  of  amyloid  material  doubtful. 


PATHOLOGIC    PROCESS]  S  -u 

The  material  may  be  carried  by  the  1>I 1  in  a  "preamyloid" 

soluble  form  to  the  tissues,  where  it  is  modified  and  deposited,  be- 
coming ilic  insoluble  resistive  amyloid  substance,  though  it  is 
possible  thai  in  some  localities  ii  may  be  formed  in  situ;  hence 
ii  is  variously  called  an  "infiltration"  or  a  "degeneration." 

It  will  be  noted,  then,  that  the  chemical  nature  of  the  four 
"all uiminous  degenerations;"  viz.,  mucoid,  colloid,  hyaline,  and 
amyloid,  is  hoi  definitely  known,  and  probably  varies  much  in 
different   cases. 

Etiology. — Toxins  of  certain  chronic  infectious  processes,  espe- 
cially those  formed  in  prolonged  suppurating  conditions  (particu- 
larly tuberculous  and  syphilitic)  of  bones,  though  suppurative 
and  ulcerative  conditions  of  various  kinds,  as  gastrointestinal, 
actinomycotic,  etc..  may  also  cause  amyloid  degeneration. 

Aseptic  suppuration,  as  by  injection  of  turpentine,  may  also 
cause  it. 

The  injection  of  toxins  alone,  as  in  preparation  of  diphthe- 
ritic antitoxin,  and  the  toxins  of  nonsuppurative  syphilitic  condi- 
tions likewise  cause  it. 

It  sometimes  occurs  without  apparent  cause. 

Locations. — The  condition  may  be  general  (amyloidosis)  or  lo- 
cal. The  organs  most  frequently  affected  are  the  kidney,  liver, 
and  spleen;  next  in  frequency,  the  larger  blood  vessels,  intestinal 
mucosa,  and  lymph  nodes,  and  less  frequently  the  stomach  and 
colon,  suprarenals,  pancreas,  heart,  etc. ;  rarely  the  lungs  or  cen- 
tral nervous  system. 

Gross  Anatomy. — An  amyloid  organ  is  enlarged  uniformly  (oc- 
casionally an  amyloid  liver  becomes  enormous)  dense,  pale,  in- 
elastic or  doughy,  sometimes  pitting  on  pressure.  The  specific 
gravity  is  increased. 

The  amyloid  material  has  a  glistening,  waxy,  translucent  ap- 
pearance. In  cut  sections,  the  surface  is  smooth,  dry  and  glossy, 
the  cut  edges  remain  sharp,  and  the  parenchyma  neither  con- 
tracts nor  protrudes.  It  is  customary  in  examining  gross  speci- 
mens at  autopsy  to  apply  iodine  (Lugol's). 

The  waxy  material  is  not  always  uniformly  distributed;  in 
the  spleen  it  may  be  confined  to  the  Malpighian  bodies,  which 
stand  out  in  round,  transparent  bodies,  looking  like  grains  of 
boiled  sago  (sago  spleen);  when  the  process  is  diffuse,  the  spleen 


58  GENERAL   PATHOLOGY 

looks  bacony   (bacony  spleen).     In  the  kidney,  it   appears  first 
in  the  glomeruli. 

Pathologic  Histology. — The  material  is  always  found  in  the 
connective  1  issue;  is  usually  found  in  the  capillaries,  in  the  media 
and  basement  membrane  of  intima  in  case  of  larger  vessels;  the 
lumen  of  the  blood  vessels  is  usually  narrowed  or  obliterated. 
The  amyloid  material  is  deposited  between  the  cells,  which  are 
pushed  aside  and  atrophied,  and  disappear  as  the  process  ad- 
vances. The  amount  of  amyloid  substance  varies  from  slight 
deposits  to  such  large  quantities  as  to  cause  disappearance  of 
the  original  elements  from  large  areas  of  the  diseased  part. 

Under  the  microscope,  the  amyloid  in  a  section  of  liver  is 
found  in  the  intermediate  zone  of  the  lobule  (i.e.,  between  the 
central  and  perilobular  zones)  as  a  pale  homogeneous  material 
following  the  course  of  the  capillaries,  and  taking  the  charac- 
teristic stain:  from  this  zone  it  gradually  spreads  until  the  whole 
lobule  is  affected. 

In  the  kidney,  the  capillary  tufts  are  first  affected,  later  the 
vessels  and  interstitial  tissues;  rarely  the  tubules  are  said  to 
contain  it,  though  in  most  cases  this  material  is  hyaline  or 
other  exudative  material  and  not  true  amyloid. 

In  the  spleen,  the  Malpighian  bodies  alone  may  be  affected, 
or  the  reticular  framework  may  be  generally  involved. 

Reactions. —  Amyloid  is  insoluble  in  water,  acids,  alkalies,  and 
very  resistant  to  bacterial  decomposition. 

It  stains  a  dee])  mahogany  brown  with  iodine,  other  tissues, 
yellow;  if  afterward  treated  with  dilute  sulphuric  acid,  it  usu- 
ally turns  brown  or  blue,  or  may  merely  turn  a  deeper  brown. 
This  iodine  reaction  fails  in  specimens  that  have  been  kept  some 
time  in  preserving  fluids,  or  that  have  become  strongly  alkaline: 
in  fact,  the  blue  reaction  is  usually  given  well  only  by  splenic 
amyloid,  or  by  the  "amyloid  bodies." 

Gentian  violet,  or  methyl  violet  (and  to  a  less  degree  also 
other  basic  aniline  dyes)  stain  the  amyloid  material  a  pink  color, 
or  pale  red  often  with  a  violet  tinge;  the  other  tissues  stain  the 
natural  violet  color. 

Pathologic  Physiology. — Xo  impairment  of  function  occurs  if 
Hie  material  is  small  in  amount:  if  large,  pressure  causes  atrophy 
and  diminished  function,  or  thrombosis  in  the  blood  vessels. 


PATHOLOGIC    PROC]  3S  59 

Results. — The  process  is  irremediable;  and  [f  progressive,  leads 
to  death.  It  may  also  pass  into  fatly  degeneration,  caseation, 
or  calcification.  Slighl  amounts  may  be  absorbed,  learned  by  ex- 
perimentally extirpating  a  part  of  a  diseased  (amyloid)  area  of 
an  organ,  and  some  time  afterward  again  examining  at  necropsy. 

The  "amyloid  bodies,"  or  corpora  amylacea,  found  in  the  pros- 
tate, lungs,  kidney,  brain,  and  posterior  cord,  also  sometimes  in 
inflammatory  areas,  in  infarcts,  granulomata,  and  neoplasms,  are 
small  concentrically  striated  bodies,  resembling  starch  granules, 
which  nearly  always  react  with  the  iodine-sulphuric  aeid.  giving 
a  blue  color,  though  sometimes  they  fail  to  react  typically.  Many 
believe  these  bodies  to  be  hyaline,  others  colloid  in  nature.  Path- 
ologically they  are  not  significant,  occurring  also  in  health. 

Infiltrations 

Infiltrations  are  simple  retrograde  processes  in  which  there  is 
deposited  within  the  cells  and  intercellular  tissues  substances 
that  are  abnormal  in  kind  or  quantity. 

Fatty  Infiltration 

Fatty  infiltration  is  an  abnormal  deposition  of  fat  within  the 
cells  of  a  part.  The  process  does  not  differ  essentially  from  the 
normal  physiologic  deposit  of  fat,  and  is  considered  pathologic 
only  when  in  excess  or  when  deposited  where  it  does  not  normally 
appear.     (Fig.  10.) 

Etiology.- — 1.  Ingestion  of  more  fat-forming  foods — fats  and 
carbohydrates — -than  the  body  needs. 

2.  Sulfoxidation  probably  accounts  for  nearly  all,  if  not  all, 
the  remaining  cases,  as  in  tuberculosis,  carcinoma,  inactivity, 
senility,  alcohol,  diabetes,  etc. 

Types. — 1.  General  fatty  infiltration,  as  obesity,  adiposity  or 
polysarcia.     2.  Local  fatty  infiltration,  as  in  heart,  etc. 

Locations. — 1.  Connective  tissues;  (a)  General  deposits,  as  in 
subcutaneous,  submucous  and  subserous  tissues.  Obesity,  belongs 
here.  Tissues  that  are  never  involved  are  the  eyelids,  ears,  ala?, 
nasi,  lips  ami  external  <renitals.  Tissues  rarely  involved  are  the 
lungs  and  central  nervous  system,  (b)  Local  deposits — found 
usually  along  the  fascia1  and  trabecular  lines  of  parts  or  organs, 


00 


GENERAL   PATHOLOGY 


as  heart,  kidney,  pancreas,  old  necrotic  foci,  degenerated  or 
sclerosed  organs,  etc. 

2.  Glandular  epithelium — practically  limited  to  liver  cells.  "In 
liver  the  connective-tissue  cells  are  not  involved,  but  the  liver 
cells.  In  all  other  parts  of  the  body,  the  connective  tissue  cells 
are  involved." — Adami. 

Gross  Anatomy. — The  part  or  organ  is  enlarged  (sometimes 
double),  tense,  and  elastic,  yellow  in  color  which  may  be  modified 
by  other  factors  and  the  sharp  edges  rounded. 


Fig.    10. — Fatty    infiltration    of    the    liver.       (Stengel    and    Fox.) 

Section  may  show  minute  fat  droplets,  and  present  a  uniform 
yellow  surface;  or  yellow  streaks  as  is  usually  the  case  in  fatty 
infiltrated  heart. 

Pathologic  Histology. — Large  globules  appear  in  the  cells  of 
connective  tissues,  or  in  hepatic  cells.  The  protoplasm  is  usually 
clear  and  of  normal  appearance.  The  nuclei  stain  well,  showing 
that  they  are  not  involved,  but  they,  as  well  as  the  protoplasm, 
are  apt  to  be  pushed  to  one  side  of  the  cell,  giving  the  "seal- 
ring"  or  "signet-ring"  appearance.  The  cell  wall  is  distinct, 
and  often  bulged. 

In  the  liver,  the  infiltration  begins  in  the  cells  at  the  periphery 
of  the  lobule,  and  proceeds  toward  the  center  as  the  process  ad- 
vances. 

Reactions. — They  are  the  same  as  in  fatty  degeneration. 


PATHOLOGIC    PROCESSES  <il 

Pathologic  Physiology. — Function  is  aol  impaired  excepl  when 
infiltration  is  extensive  enough  to  cause  pressure. 

Results.  Recovery  takes  place  by  absorption,  if  the  infiltration 
is  slight  or  even  moderate.  It'  extensive  or  of  long  standing,  it  is 
followed  by  fatty  degeneration  or  necrosis. 

Table  of  Differences  Between  Fatty  Infiltration  and  Fatty 
Degeneration 

Fatty  Infiltration  Fatty  Degeneration 

Deposit  of  fal  in  healthy  cells.  Deposit    in    diseased    cells. 

Globules  of  fat  usually  large.  Globules  usually  small. 

Nuclei    uninvolved,    staining   well.  Nuclei  involved,  staining  poorly. 

Cytoplasm    healthy    and    capable    of  Cytoplasm  degenerated, 
resuming   function   if   fat    be    ab- 
sorb '1. 

Nucleus   and    cytoplasm     apt    to    l>e  Nucleus  not  displaced, 
pushed  to  one  side — "signet  ring." 

Condition    not   necessarily   serious.  Always  serious. 

Pigmentary  Infiltration 

Pigmentary  infiltration  is  an  abnormal  deposit  of  pigment 
within  or  between  the  cells  of  any  tissue. 

Etiology. — I.  Extraneous  pigments  (those  of  external  origin) 
are  derived  from:  1.  Inhalation  of  smoke  and  dust  particles  of 
all  kinds,  causing  pneumonokoniosis  or  "lung  dust  disease." 

2.  Ingestion  of  dust  and  substances  like  soluble  salts  of  silver, 
especially  the  nitrate,  also  lead  salts,  etc. 

3.  Implantation  and  absorption  by  skin,  as  in  tattooing,  and 
possibly  lead,  copper,  etc. 

II.  Pigments  of  internal  origin  are  due  to: 

1.  Disintegration  of  hemoglobin  (hemolysis)  either  directly  in 
the  tissues,  or  in  the  blood  vessels  when  the  blood  is  hemolyzed 
by  venins,  toxins,  poisons,  anemias,  cachexias,  etc.,  (hematog- 
enous pigmentation)  ;  or  indirectly,  when  the  blood  pigment  is 
converted  into  bile  pigment  in  the  liver,  but  instead  of  escaping 
as  normally  through  the  hepatic  ducts  with  the  bile,  should  these 
ducts  become  obstructed  by  catarrhal  or  other  conditions,  the 
bile  pigments  are  forced  into  the  lymph  vessels  (and  to  a  less 
extent  into  the  blood  vessels)  and  carried  to  the  tissues  through- 
out the  body  (hepatogenous  pigmentation). 


62  GENERAL    PATHOLOGY 

2.  Malarial  pigmentation.  This  is  probably  formed  by  the  ac- 
tion of  the  Plasmodium  malaria?  upon  the  red  blood  cells,  liberat- 
ing and  modifying  the  hemoglobin  or  hematin. 

3.  Metabolic  pigmentation.  Certain  cells  elaborate  the  pig- 
ment out  of  protein  substances  possibly  by  action  of  intracellular 
oxidases  upon  the  aromatic  groups  of  the  protein  molecule  (von 
Furth's  theory). 

Such  pigment  appears  normally  in  skin,  hair,  choroid  and 
retinal  coats  of  the  eye,  in  pregnancy  (chloasma  uterinum)  and 
pathologically  in  certain  tumors,  in  the  shin,  etc. 

The  term  melanin  is  applied  to  all  these  pigments  though  they 
vary  much  in  composition,  some  being  iron  or  sulphur  free,  while 
some  contain  small  amounts  of  iron,  and  some  contain  sulphur 
in  variable  amounts  up  to  10  per  cent  in  melanosarcomata. 

Lipochromes,  or  pigments  of  fatty  origin,  are  usually  classed 
as  metabolic  pigments,  but  their  nature  and  formation  are  not 
well  understood ;  they  occur  normally  in  fats,  in  the  corpora 
lutea  (lutein)  and  pathologically  in  lipomata,  xanthomata,  (pale 
yellow),  in  chloromata  (green),  in  certain  nerve  cells  in  old  age, 
and  possibly  in  brown  atrophy  of  muscle  cells  (but  this  has  also 
been  classed  as  hematogenous  in  origin.) 

4.  Parasitic  pigmentation.  Some  bacteria  and  moulds  form 
various  pigments. 

Locations. — Mueh  of  the  inhaled  pigment  probably  never 
reaches  the  alveoli  of  the  lungs,  but  is  caught  by  the  bronchial 
ciliated  epithelium  and  in  part  coughed  up,  though  part  is  car- 
ried into  the  submucous  tissue,  where  some  remains  permanently 
and  the  remainder  is  conveyed  by  the  lymphatics  to  the  nearest 
glands,  as  peribronchial  and  even  mediastinal  glands  and  sub- 
pleural  spaces.  In  rare  cases  the  pigment  reaches  the  general 
circulation  and  is  deposited  in  the  kidney,  liver,  spleen,  and 
alimentary  mucosa. 

Ingested  pigments  are  likewise  deposited  in  the  alimentary 
mucosa  and  adjacent  glands,  or  as  in  silver  discoloration  are  dif- 
fusely distributed  between  the  cells  of  the  internal  organs  and 
1  issues,  and  in  the  subepithelial  layer  of  the  skin,  where  de- 
posited in  the  form  of  silver  albuminate,  it  is  finally  reduced, 
resulting  in  a  bluish  pigment. 


PATHOLOGIC    PROi  63 

In  chronic  lead  poisoning,  the  blue  line  on  the  gums  is  due  to 
th«>  formation  of  lead  sulphide. 
In  tattooing,  the  pigments  are  Pound  in  the  deep  layers  of  the 

skin,  and  in  the  adjacent  lymphatic  glands. 

Hematogenous  pigmentation  may  he  (a)   general  or  (b)  local. 

(a)  In  the  general  form,  blood  is  hemolyzed,  liberating  hem- 
oglobin into  the  blood  stream  (hemoglobinemia)  j  as  much  of  this 
a^  can  be  disposed  of  by  the  liver  is  converted  into  bile,  while  the 
remainder  is  excreted  by  the  kidneys  (hemoglobinuria)  wholly 
or  in  pari  ;  in  the  latter  case  some  hemoglobin  is  broken  up  and 
deposited  in  various  tissues.  This  is  best  seen  in  the  liver  (espe- 
cially in  periphery  of  lobules),  spleen  and  kidneys. 

(b)  In  the  local  form,  as  in  thrombosis,  and  interstitial  hemor- 
rhages (including  bruises),  blood  escapes  into  the  tissues,  is  in 
part  eliminated  and  in  part  vailed  off  and  and  coagulated;  the 
hemoglobin  diffuses  out  and  is  broken  up  into  the  various  deriva- 
tives of  blood  pigments  in  situ.  The  different  shades  of  color  from 
red  or  brown  to  black  depend  upon  successive  degrees  of  re- 
ductions of  the  pigments. 

Local  pigmentation  is  seen  in  infarcts,  hematomata,  thrombi, 
extravasations,  etc. 

A  dark  or  black  pigmentation,  resembling  melanin  ("pseudo- 
melanin")  is  often  seen  in  the  abdominal  region  of  dead  bodies, 
due  to  sulphide  of  iron  (H2S  from  gastrointestinal  decomposition 
acting  on  the  iron  derived  from  the  blood).  It  may  become  more 
or  less  general  in  distribution,  and  also  sometimes  forms  during 
life  in  and  around  gangrenous  areas,  and  other  localities  where 
free  or  loosely  bound  iron  and  H2S  come  together. 

The  greenish  discoloration  in  the  abdominal  region  of  dead 
bodies  is  due  to  sulphur-hemoglobin,  due  to  H2S  plus  undecom- 
posed  hemoglobin. 

Hepatogenous  pigmentation  (jaundice)  is  found  either  in  the 
tissues  in  solution  or  in  crystal  form  (needles  or  rhombic  plates) 
especially  in  liver,  skin,  mucous  membrane,  serous  membrane  and 
glandular  and  fatty  tissues  generally,  less  often  in  other  tissues — 
the  brain  substance  alone  escaping. 

Malarial  pigment  is  found  in  various  tissues,  especially  in  spleen, 
liver,  kidney,  bone  marrow  and  brain. 

Metabolic   pigments   are   found   locally    in    certain    tumors,    as 


64  GENERAL   PATHOLOGY 

melanotic  sarcomata  and  carcinomata,  pigmented  moles,  chloas- 
mic  spots,  etc.,  and  generally  in  the  skin  in  Addison's  disease, 
revere  anemias  and  cachexias,  abdominal  tuberculosis,  abdominal 
tumors,  and  senility. 

Lipochromes  occur  as  stated  under  etiology,  and  parasitic  pig- 
ments are  found  in  the  various  tissues  invaded  by  the  organisms. 

Gross  Anatomy. — Discoloration  is  seen  as  follows: 

In  Lungs : 

(1)  Dark  or  black  in  anthracosis  (coal  dust,  smoke,  etc.)   as  in  coal  miners. 

(2)  Grayish  in  chalicosis  (stone  dust)   as  in  stonecutters. 

(3)  Brownish  red  in  siderosis   (iron  dust)   as  in  iron  workers. 

(4)  Grayish  in  calcicosis   (lime  dust)    as  in  marble  cutters. 

(5)  Grayish  in  silicosis  (silica  dust)  as  in  glass  cutters. 
(6")  Yellowish  in  aluminosis   (clay)   as  in  potters. 

(7)   Rusty  brown  in  tabacosis  (tobacco  dust),  etc. 
In  skin  ;  also  gastrointestinal  walls,  kidney,  liver,  etc. 

Bluish  color  in  argyria  due  to  AgNO    and  other  soluble  salts  and  silver. 

Rarely  other  extraneous  pigments  cause  discolorations,  as  in  lungs. 
Hematogenous  pigments  if  in  sufficient  amount  will  color  the  tissues: 

(1)  Reddish  brown  when  due  to  hemosiderin  and  hematoidin. 

(2)  Dark  or  black  when  due  to  iron  sulphide. 

(3)  Dark   or   black   when   due   to  malarial  pigment. 
Hepatogenous  pigments : 

(1)  Yellowish  red,  when  due  to  bilirubin. 

(2)  Yellowish  green  when  due  to  biliverdin   (oxidized  bilirubin). 
Metabolic  pigments  appear  (pathologically); 

(1)  Dark  brown  or  black  in  tumors,  etc.,  due  to  melanin. 

(2)  Yellowish  brown  in  skin. 

(3)  Yellow,  brown  or  green  in  tumors,  etc.,  due  to  lipochromes. 
Parasitic  pigments  are  of  various  colors  as 

blue  in  B.  pyocyaneus;  yellow  in  Actinomyces  bovis;  black  in  Mucor  niger 
(on  lingual  papilla?)  ;   brown  in  Microsporon  furfur   (tinea  versicolor)  ;   etc. 

Pathologic  Histology. — By  transmitted  light,  extraneous  pig- 
ments appear  black,  and  usually  coarsely  granular  and  extra- 
cellular, though  leucocytes  are  apt  to  contain  them  (phago- 
cytosis). 

Hemosiderin  appears  as  intracellular  (less  often  extracellular) 
fine  irregular  granules  of  yellowish  or  reddish  brown  color  in 
various  tissues,  but  is  best  seen  in  liver,  spleen  and  lungs,  fol- 
lowing congestion.  A  certain  amount  of  oxygen  seems  to  be 
necessary  in  its  formation,  therefore  it  is  seen  at  the  periphery 
of  old  necrotic  areas,  as  blood  clots,  infarcts,  etc. 


PATTTOTiOCIC    PROCESSES 


65 


Fig.    11. — Anthracosis  of   the  lung.      (Delafield  and   Prudden.) 


66  GENERAL    PATHOLOGY 

Hematoidin  appears  in  fine  acicnlar  crystals  or  rhombic  plates, 
or  spherical  granules,  usually  a  bright  yellowish  red,  always  be- 
tween cells  and  oftenest  in  the  center  of  old  blood  clots  or  in- 
farcts.    Oxygen  must  be  absent  when  it  is  formed. 

Iron  sulphide  appears  as  black  granules. 

Bilirubin,  bilifuscin  and  biliverdin  usually  appear  as  fine 
granules,  occasionally  as  crystals,  yellowish  to  brown  in  color, 
intracellular,  pigmenting  the  nucleus  as  well  as  the  cytoplasm 
and  are  best  seen  in  liver. 

Malarial  pigment  is  a  black,  finely  granulated  pigment,  found 
in  the  perivascular  lymph  spaces  in  organs  and  tissues,  especially 
of  the  spleen,  liver,  kidney,  and  brain,  also  in  the  cells  of  these 
organs  at  times  and  in  phagocytes. 

Melanin  is  seen  as  coarse  granular,  brownish  black  pigment 
in  various  tissues,  as  in  melanosarcomata,  usually  within  the 
cells  though  sometimes  free  in  lymphatic  spaces ;  in  marked  cases 
it  may  appear  in  the  blood  (melanemia)  and  be  excreted  in  the 
urine  (melanuria)  either  as  melanin,  or  as  melanogen  (colorless) 
which  darkens  (oxidizes)  on  standing. 

Lipochromes  are  seen  within  the  cells  of  tumors,  etc.,  and 
stain  with  the  ordinary  fat  stains. 

Reactions. — Hemoglobin  is  composed  of  globin  (protein)  96 
per  cent  and  hematin  4  per  cent.  The  latter  contains  the  coloring 
matter  of  the  blood. 

The  two  principal  derivatives  of  hematin  are  hemosiderin 
(iron-containing)  normally  used  for  reconstructing  hemoglobin, 
and  hematoidin  (iron  free)  isomeric  with  bilirubin,  and  nor- 
mally eliminated. 

Hemosiderin  is  colored  blue  (Prussian  blue)  when  sections  are 
treated  with  potassium  ferrocyanide,  2  per  cent  aq.  sol.  followed 
by  HC1  0.5  per  cent  in  glj-cerin,  or  1  per  cent  in  alcohol  (Perl's 
test).  Hematoidin  will  not  respond  to  Perl's  test — since  it  con- 
tains no  iron;  hemoglobin  will  not,  because  its  iron  is  too  firmly 
united  with  the  protein. 

Bile  pigments  give  the  Gmelin's  reaction — a  play  of  colors; 
viz.,  green,  blue,  violet,  red  and  yellow,  when  adding  a  drop  of 
commercial  nitric  acid.  They  also  turn  green  with  weak  tincture 
of  iodin.    Hematoidin  also  responds  to  Gmelin's  test. 


PATHOLOGIC    PROCESSES  67 

Lipochromes  are  colored  by  Sudan  in  and  Scharlach  R,  and 
usually  by  osmic  acid. 

Extraneous  pigments  are  usually  insoluble;  those  soluble  in 
acids  evolve  C02.  Carbon  is  distinguished  from  melanin  and 
other  dark  pigments  by  its  insolubility  in  strong  H2S04. 

Pathologic  Physiology.— Large  amounts  of  pigment  may  cause 
proliferation  of  connective  tissues  with  atrophy  of  the  paren- 
chyma, and  consequent  loss  of  function. 

Results. — Pneumonokoniosis  is  often  followed  by  tuberculosis. 
Fibrosis  follows  nearly  all  forms  of  extraneous  pigmentation. 

Internal  pigments  are  apt  to  become  absorbed  in  time,  though 
in  some  cases  they  become  encapsulated. 

Albinism  is  a  deficiency  or  absence  of  normal  amount  of 
melanotic  pigment.  Leukoderma  is  an  irregular  distribution  of 
pigment  in  the  skin,  some  parts  paler,  others  more  pigmented. 
Canities  is  grayness  or  whiteness  of  hair,  due  to  loss  of  color, 
probably  resulting  from  decrease  or  loss  of  intracellular  oxida- 
tion of  the  chromogen. 

Calcareous  Infiltration 

Calcareous  infiltration  is  the  abnormal  deposit  of  earthy  salts 
in  the  tissues,  chiefly  phosphates  and  carbonates  of  calcium, 
though  magnesium  salts  are  also  found.     (Fig.  12.) 

Etiology. — Necrosed  or  diseased  tissue  seems  necessary  (with 
the  possible  exception  of  the  calcareous  metastases).  The  min- 
eral matter  in  solution  is  brought  by  the  blood  and  lymph  to 
the  part,  and  by  some  local  chemical  process  is  deposited  in  in- 
soluble form. 

At  present  there  is  a  tendency  to  consider  that  from  the  local 
disintegrated  tissues,  protein  substances  arise  which  unite  with 
the  calcium  and  magnesium,  and  subsequently  are  replaced  by 
phosphoric  and  carbonic  acids  to  form  the  corresponding  salts; 
or  that  the  fatty  acids,  liable  to  appear  in  degenerated  areas, 
may  form  calcium  and  magnesium  soaps  and  may  likewise  be  re- 
placed by  the  stronger  acids. 

Calcareous  metastasis :  In  some  rare  cases  of  resorption  of 
bone,  as  in  extensive  caries,  osteomalacea,  osteosarcoma,  etc., 
there  may  be  widespread  deposition  of  salts  in  cartilage,  lungs, 
gastric  mucosa,  arterial  and  capillary  walls,  etc.    The  tissue  here 


68 


GKXERAL    I'ATIIOI.OOY 


is  not  known  to  have  been  previously  diseased,  though  some 
claim  that  the  deposit,  being  intercellular,  is  "in  inert  or  dead 
tissue."  Senile  calcification  of  blood  vessels,  etc.,  has  been 
classed  as  metastatic  since  bone  is  absorbed  in  old  age.  but  this 
depends  probably  upon  the  hyaline  changes  occurring  in  senile 
sclerosis. 

Locations. — Sclerotic  vessel  walls,  especially,  aorta,  coronary, 
cerebral,  radial,  etc. 


Fig.    12. — Calcareous   in  filtration   of   the  wall   of  a   small   artery   from   the   wall   of  a  gumma 
of  the  liver.     Zeiss,  Oc.  2;  ob.  D.  D.   (McFarland.) 


Endocardium  (especially  of  valves);  pericardium,  myocardium, 
etc. 

Pituitary  body:  meninges;  ventricular  plexus;  ganglion  cells,  etc. 

Necrotic  foci,  as  tubercular,  parasitic,  etc. 

Sclerotic  foci,  as  sears,  infarcts,  or  thrombi. 

Joints. 

Tumors,  especially  the  avascular,  as  fibroma  (particularly 
uterine),  and  tumors  involving  bone  and  cartilage;  also  cysts. 
goiters,  psammomata,  etc. 

Long  retained  dead  fetuses  (lithopedia). 


PATHOLOGIC    PROCESSES  69 

Concretions  within  the  organs  or  their  duds,  as  tonsils,  pros- 
tate, etc. 

Gross  Morbid  Anatomy.  -When  the  deposit  is  abundant,  the 
parts  are  hard  and  brittle,  of  white,  gray,  or  yellow  color  and 
opaque  appearance.  The  lesions  are  gritty  to  the  touch  and 
section  knife.  Old  tuberculous  calcified  areas  are  apt  to  be  sur- 
rounded by  pigmented  fibrous  tissues,  especially  in  lungs  and 
bronchia]  glands. 

Pathologic  Histology. — Fine  intercellular  granules,  less  often 
intracellular  (as  in  the  ganglion  cells)  are  seen,  appearing  black 
by  transmitted,  and  white  and  glistening  by  reflected,  light.  By 
coalescence,  larger  masses  form,  usually  with  concentric  layers. 
In  blood  vessels,  serous  membrane,  etc.,  calcareous  plates  are 
seen.     When  intracellular,  the  cells  show  degeneration. 

Reactions. — Acids  will  dissolve  the  granules,  and  in  case  of 
carbonates  with  evolution  of  gas  (C02),  observable  under  the  mi- 
croscope by  running  5  per  cent  IIC1  solution  under  cover-slip. 
To  differentiate  between  lime  and  other  salts  soluble  in  HC1, 
add  concentrated  BuSO^,  which  forms  needles  of  CaSO^  (gyp- 
sum). Lime  salts  stain  blue  with  hemotoxylin,  and  black  with 
AgN03. 

Pathologic  Physiology. — Function  is  impaired  or  destroyed  by 
pressure,  or  inflammatory  conditions  are  caused  by  irritation. 
In  calcified  blood  vessels,  nutrition  to  various  tissues  is  re- 
stricted. 

Results. — Very  small  deposits  may  be  absorbed,  but  usually 
there  is  proliferation  of  connective  tissue,  with  capsule  forma- 
tion. Sometimes  degeneration  of  adjacent  tissues  is  caused  by 
the  calcareous  masses. 

Ossification. — Ossification  which  is  the  deposition  of  lime  salts 
in  a  uniform  regular  order,  as  in  normal  bone  formation,  by  the 
activity  of  certain  cells  (osteoblasts)  occurs  pathologically  in 
tumors  connected  with  cartilage,  bone,  and  periosteum,  and  in 
ossifying  inflammation  of  muscles  (myositis  ossificans). 

Concretions  or  Concrements 

"While  calcareous  infiltration  is  a  deposit  within  tissues,  con- 
cretions are  deposits  of  lime  and  other  substances  within  the 
ducts  and  cavities  of  the  body. 


"0  GENERAL    PATHOLOGY 

In  the  formation  of  concretions  there  is  always  a  small  mass 
of  mucus,  desquamated  epithelium,  secretory  mailer,  parasites 
or  foreign  bodies;  in  other  words,  usually  some  pathologic  prod- 
uct upon  which,  as  a  nucleus,  the  various  salts  or  substances 
forming  the  hulk  of  the  concretion  are  deposited,  "much  as  cane 
sugar  crystallizes  on  a  string  to  form  rock  candy,  but  with  the 
important  exception  that  the  concretions  are  mixed  with  mucin 
or  other  organic  matter  which  remains  as  a  frame  work  when 
the  salts  are  dissolved  out." 

Gallstones  (biliary  calculi)  are  made  up  of  variable  amounts 
of  cholesterin,  the  chief  constituent  of  the  great  majority  of 
these  stones,  and  of  bile  pigments  and  calcium.  Renal  calculi 
kidney  stones)  are  composed  of  uric  acid,  oxalate  of  lime,  or 
phosphates;  less  frequently  of  other  substances.  Vesical  cal- 
culi (of  the  urinary  bladder)  are  composed  of  phosphates,  uric- 
acid,  and  oxalates  of  lime  ;  rarely  of  other  substances. 

Calcium  salts  form  the  chief  mineral  constituent  of  rhinoliths. 
broncholiths,  phleboliths  (which  are  calcification  of  organized 
thrombi;  often  found  in  the  prostate  or  uterus),  salivary,  ton- 
sillar, lacrimal,  cutaneous,  appendicular,  pancreatic  and  preputial 
concretions  and  prostatic  calculi.  In  the  intestines,  concretions 
or  enteroliths,  usually  consist  of  ammonio-magnesium  phosphates, 
though  the  finer  "intestinal  sand"  consists  of  calcium.  Occa- 
sionally concretions  of  fat  and  soaps  may  follow  the  ingestion 
of  large  doses  of  olive  oil,  and  be  mistaken  for  gallstones. 

Hydropic,  Dropsical,  or  Serous  Infiltration 

Hydropic  infiltration  is  an  excess  of  fluid  within  the  cells  in 
the  form  of  globules.  It  must  be  distinguished  from  edema, 
dropsy,  or  anasarca,  which  is  due  to  an  outpouring  of  serum  from 
the  blood  vessels  into  the  tissues  to  an  abnormal  decree,  while 
in  hydropic  infiltration  certain  cells  imbibe  more  fluid  than  nor- 
mal, though  the  lymph  surrounding  them  may  not  lie  abnormal  in 
quantity.     (Fig.  13.) 

Etiology. — The  etiology  is  not  definitely  known,  apart  from 
a  disturbed  osmotic  pressure,  which  may  be  due  to  "dissociation 
of  the  colloids,  whereby  crystalloids  are  liberated  into  the  cyto- 
plasm" causing  endosmosis  of  lymph.  Toxins  are  probably  a 
causal  factor,  at  least  in  some  cases  (smallpox). 


PATHOLOGIC    PROCESSES 


71 


Gross  Morbid  Anatomy.  II'  abundant,  the  pari  is  enlarged, 
soft,  and  boggy. 

Pathologic  Histology. — Vacuoles  of  varying  sizes,  containing 
serous  fluid,  arc  seen  in  the  cells,  which  are  enlarged  and  in  some 
cases  ruptured. 

Tn  edema  the  cells  also  may  contain  fluid,  i.e.,  edema  may  be 
accompanied  by  hydropic  infiltration. 

Locations. — Any  type  of  cells  may  be  affected,  but  most  com- 
monly the  epithelial  cells,  as  those  of  mucous  membranes,  glan- 
dular viscera,  epithelial  tumors,  etc. 

Results. — This  condition  is  not  serious,  unless  very  extensive. 


Fig.  13. — Dropsical  infiltration  of  the  epithelial  cells  of  a  carcinoma  of  the  breast:  a, 
ordinary  epithelial  cells;  b,  b,  dropsical  cells;  c,  dropsical  nuclei;  d,  enlarged  nucleoli, 
i  Ziegler.) 

Glycogenic  or  Glycogenous  Infiltration 

Glycogenic  infiltration  is  an  infiltration  of  glycogen  in  cells 
normally  free  from  it.  or  an  excessive  deposit  in  cells  which 
normally  contain  it. 

Etiology. — The  cause  of  pathologic  deposits  is  not  known. 

Locations. — In  diabetes  (in  which  disease  it  is  most  frequently 
found)  glycogen  occurs  in  the  renal  epithelium,  heart  muscle, 
liver,  and  leucocytes.  In  tumors,  it  occurs  within  the  tumor  cells, 
especially  those  of  malignant  connective  tissue  tumors.  In  septic 
and  inflammatory  conditions,  the  local  cells  and  leucocytes  are 
affected.  Glycogen  granules  may  also  be  found  free  in  the  blood 
stream. 

Gross  Morbid  Anatomy. — Sometimes  an  organ  is  slightly  en- 
larged; often  there  is  no  change. 


fZ  GENERAL    PATHOLOGY 

Pathologic  Histology- -Small  globules  or  granules  are  seen  usu- 
ally within  the  cells,  but  sometimes  also  between  the  cells,  or 
even  free  in  the  blood  or  in  fluid  exudates.     The  intracellular 
granules  are  usually  near  the  nuclei,  which  are  usually  well  pre- 
ed,  even  in  advanced  cas 

Reactions.— Soluble  in  water,  the  granules  are  dissolved  and 
leave  empty   3  when  sections  are  treated  with  water;  the 

margins  of  these  -       ;es  for  some  unknown  reason  tend  to  take 
the  basic  stain-.     To  preserve  the  glycogen  in  the  tissues,  the 
latter  must  be  fixed  in  alcohol     in  which  glycogen  is  insoluble 
and  rapidly — because  the  granules  quickly  change  into  glue 
after  death  of  the  tissue. 

Glycogen  stains  mahogany  brown  as  does  amyloid)  or  wine 
color  with  iodine  dissolved  in  glycerin,  or  in  the  form  of  the 
tincture  diluted  with  four  parts  of  absolute  alcohol.  No  blue 
color  is  produced  on  adding  II _>'  I  .  The  brown  color  disappear- 
on  heating,  or  on  addition  of  alkalies,  but  reappears  respectively 
on  cooling  or  acidifying. 

Ptyalin  rapidly    converts  glycogen  into  dextrose,  and  may  be 
section,  showing  microscopically  whether  the  granules 
are  glycogen. 

Pathologic  Physiology. — Normally  glycogen  is  formed  within 
the  cells  by  intracellular  enzymes,  which  dehydrate  and  poly- 
merize the  sugar  brought  by  the  blood.     The  liver  and  the  mus- 

-  are  the  chief  normal  storehouses  of  glycogen,  which  when 
needed  by  the  tiss  -  -  again  converted  into  dextrose  by  a  re- 
verse enzymotic  process.  Pathologically,  glycogen  is  diminished 
or  absent  from  the  normal  situations,  and  appears  in  excess  in 
other  locations. 

The  result  is  always  serious,  since  the  accompanying  or  causal 
conditions,  as  diabetes,  malignant  tumor.  re  usually  fatal. 

Necrosis 

Necrosis  means  death  of  tissue.     There  are  three  grades: 
1.  Necrobiosis,   or   death  of  individual  cells,   occurring  path- 
ologically in  the  various  degenerations,  and  normally  in  the  break- 
ing down  of  secreting  cells,  as  in  the  formation  of  sebum,  and 
in  other  cells,  conspicuously  the  outer  cells  of  the  epidermis. 


PATHOLOGIC    PROC1  SS]  -  7:! 

2.  Necrosis  proper,  or  death  of  a  portion  of  ;i  tissue  in  the 
midst  of,  or  attached  to,  Living  tissue. 

3.  Somatic  death — death  of  the  entire  organism. 

Necrosis  by  which  term  the  second  form  is  usually  referred* 
to — lias  the   following  general   etiology: 

1.  External  agencies,  as  heat,  cold,  electricity,  x-ray,  trauma, 
poisons,  microorganisms. 

2.  Interna]  agencies,  as  circulatory  and  nutritional  disturb- 
ances, trophic  and  vasomotor  influences,  toxins. 

These  various  causes  do  not  always  produce  the  same  type  of 
necrosis,  but  may  cause  one  form  in  some  cases,  and  another  in 
other  cases.  Any  part  of  the  body  may  he  affected.  When  in- 
volving soft  tissues,  about  to  be  detached,  the  area  is  called  a 
sphacelus,  or  slough;  when  involving  a  hone,  a  sequestrum. 

Changes  may  be  seen  in  the  intercellular  substances  and  cells; 
the  latter  become  shrunken  or  swollen,  fragmented  or  dissolved 
(cytolysis)  and  take  the  stain  very  poorly.  The  nuclei  may  show 
fragmentation  of  the  chromatin  (karyorrhexis)  with  extrusion  of 
the  fragments  into  the  cytoplasm  where  they  finally  disappear; 
or  may  retain  their  form  but  stain  less  and  less  distinctly  until 
they  dissolve  (karyolysis) ;  or  may  shrink  (pyknosis)  staining 
more  deeply,  before  they  dissolve  and  disappear. 

Fate  of  Necrotic  Tissue: 

1.  It  may  be  absorbed,  with  regeneration  of  normal  tissue,  or 
with  scar  formation. 

2.  It  may  be  retained,  and  become  encapsulated. 

3.  It  may  be  removed  en  masse  spontaneously  or  artificially. 

The  following  types  are  usually  recognized: 

Coagulation  necrosis. 

Liquefaction,  or  colliquative,  necrosis. 

Caseous  necrosis,  or  caseation. 

Fat  necrosis. 

Gangrene. 

Coagulation  Necrosis 
Coagulation  necrosis  is  death  of  tissue   in  which  the  protein 
suffers  a  change  similar  to,  or  identical  with,  coagulation  (Fig.  14). 
Coagulation  is  the  conversion  of  the  soluble  colloids  into  a:i 
insoluble  form. 


74  GENERAL   PATHOLOGY 

Etiology. — Any  of  the  general  causes  already  mentioned,  but 
especially  physical  agents,  as  heat,  cold,  and  trauma.  Loss  of 
nutrition,  as  in  infarcts.  Chemicals,  as  caustics.  Toxins,  espe- 
cially of  pyogenic  cocci,  B.  tuberculosis,  and  B.  diphtherias. 

Physical  and  chemical  agents  cause  coagulation  by  direct  ac- 
tion. In  exudates  the  action  is  analogous  to,  or  identical  with, 
blood  coagulation,  which  consists  of  the  conversion  of  fibrinogen 
(present  in  blood,  lymph  and  exudates)  into  fibrin  by  action  of 
the  thrombin  (fibrin  ferment).  The  thrombin  is  thought  to  be 
produced  when  "prothrombin"  (possibly  a  nucleo-protein  ex- 
isting in  leucocytes,  blood  platelets  and  tissue  cells,  and  liberated 
when  these  are  injured)  is  activated  by  the  calcium  salts  of  the 
blood  or  lymph. 


S 


i 


Fig.    14. — Coagulation    necrosis    of    the    hepatic    cells    in    a    case    of    puerperal    eclampsia. 

(Karl   and    Schmorl.) 

In  anemic  areas  the  tissue  cells  possibly  coagulate  from  the 
action  of  coagulins  contained  within  the  cells,  though  this  has 
never  been  actually  demonstrated.  "When  lymph  infiltrates  such 
areas,  fibrin  is  formed. 

Locations. — Seen  in  tissues  rich  in  protein,  especially. 

1.  In  bloodless  parts,  as  anemic  infarcts,  and  tubercles  in  the 
early  stages  of  tuberculosis. 

2.  In  inflammatory  exudates,  including  "false  membranes" 
upon  mucous  surfaces,  fibrinous  exudates  upon  serous  surfaces, 
around  abscesses  and  ulcers. 

3.  In  blood  clots — extravascular  or  intravascular  (thrombi),  in 
interstitial  hemorrhages  and  hemorrhagic  infarcts. 


PATHOLOGIC    PROCESSES  7.~> 

4.  Tn  striated  muscles,  in  eases  of  typhoid  and  other  fevers. 

Gross  Pathology. — The  parts  are  usually  dry,  firm,  pair,  glazed 
and  more  or  less  swollen.  Solid  tissues  present  the  appearance 
of  boiled  flesh.  Later  the  color  becomes  grayish  and  the  pari 
inclines  to  soften.  False  membranes,  which  are  a  coagulation 
necrosis  of  certain  inflammatory  exudates,  have  a  gelatinous  or 
mucoid  consistence,  and  arc  not  readily  detached  from  the  un- 
derlying tissue. 

Blood  clots  are  red  and  semifluid,  and  break  with  a  gelatinous 
fracture  when  fresh  ("currant  jelly"  clots)  ;  are  yellow  and 
gelatinous  when  leucocytes  predominate  ("chicken-fat"  clots); 
and  "white"  clots  when  the  cells  have  largely  disappeared  and 
fibrin  alone  remains. 

Pathologic  Histology. — The  cells  lose  their  staining  power 
early,  become  indistinct,  and  later  disintegrate  completely.  Mus- 
cle cells  lose  their  striae,  and  in  cardiac  muscle  the  intercellular 
cement  substance  often  dissolves  out,  and  the  fibers  separate  and 
may  present  vaeuolation  and  fragmentation.  The  nuclei  stain 
faintly  and  later  disappear. 

The  blood  vessels  at  the  margins  of  the  necrosed  area  are 
thrombosed.  In  blood  clots,  there  is  usually  more  or  less  fibrin, 
which  in  recent  clots  consists  of  a  dense  reticulum  of  fine  fibril- 
be  with  "nodal  points"  at  their  points  of  intersection.  In  older 
clots  and  in  exudates  the  nodal  points  are  not  seen,  the  fibrils 
are  less  distinct,  or  the  fibrin  may  appear  as  granules.  In  anemic 
infarcts  or  other  anemic  areas,  the  fibrin  is  very  small  in  amount 
or  may  be  wholly  absent,  and  in  any  case  may  require  special 
staining  (as  Weigert's)  to  demonstrate. 

Physiologic  function  is  usually  considerably  disturbed. 

Results. — Small  areas  may  be  liquefied  and  absorbed.  Larger 
areas  may  undergo  caseation  and  calcification,  or  may  liquefy 
and  suppurate  and  be  replaced  by  normal  tissue  or  by  scar  tis- 
sue; they  may  also  liquefy  and  become  encysted. 

Liquefaction  Necrosis 

Liquefaction  necrosis  is  death  of  a  tissue  with  transformation 
into  fluid.  It  may  be  primary,  as  in  the  central  nervous  system; 
or  secondary,  as  when  following  coagulation  necrosis,  cheesy 
necrosis,  inflammation,  gangrene,  and  tumors. 


(6  GENERAL    1'ATIIOLOGY 

Etiology. — 1.  Lysins,  or  liquefying  enzymes  are  the  causal  fac- 
tors.  Aseptic  softening-  following  proteolysis  by  enzymes  either 
from  the  dead  cells  ('autolysis)  or  from  leucocytes  (heterolysis). 
In  septic  softening,  the  bacteria  elaborate  the  lysins,  as  in  sup- 
puration, gangrene,  etc. 

In  the  central  nervous  system,  thrombosis  of  a  terminal  artery 
infarcts)  which  elsewhere  would  cause  coagulation  necrosis,  here 
causes  liquefaction  necrosis — cause  being  unknown,  probably  lack 
of  coagulins.  . 

2.  Fluids  may  infiltrate  the  Tissues  and  dissolve  them. 

Locations. — Liquefaction  necrosis  occurs  in  any  tissue.  It  is 
common  in  acute  inflammation,  abscesses,  vesicle  or  cyst  forma- 
tion,  and  in  anemic  and  hemorrhagic  infarcts  of  brain. 

Gross  Pathology. — The  tissue  is  soft,  at  first  semifluid,  pale  or 
yellow  from  fatty  material,  reddish  brown  or  greenish  from  blood 
pigments  or  bile.  Later  there  is  fluid  containing  broken  down 
cells  and  debris. 

Microscopically. — The  cells  undergo  disintegration,  fat,  choles- 
terin,  etc..  being  liberated,  resulting  in  a  fluid  debris,  containing 
granules,  and  a  few  leucocytes  which  are  sometimes  engorged 
with  fat  globules. 

Results. — The  contents  may  coagulate,  become  encysted,  be 
absorbed  or  discharged,  and  the  space  if  small,  occupied  by  nor- 
mal tissue,  or  if  larger,  by  connective  tissue  (cicatrization). 

Cheesy  Necrosis,  or  Caseation 

Cheesy  necrosis,  or  caseation  is  death  of  a  part  with  the  forma- 
tion of  a  cheese-like  material.     (Fig.  15.) 

Etiology. — Toxins,  especially  of  B.  tuberculosis.  It  may  fol- 
low coagulation,  or  as  some  state  it,  be  a  form  of  coagulation 
necrosis  of  the  proteins  with  appearance  of  a  certain  amount 
of  fat. 

Locations. — Old  tuberculous  lesions,  gummata,  blood  clots,  in- 
farcts, and  areas  of  coagulated  necrosis.  The  typical  cheesy 
necrosis  is  that  occurring  in  tuberculosis;  whether  that  which 
occurs  in  other  situations  is  true  caseation  is  still  a  disputed  point. 

Gross  Pathology. — The  area  is  pale  yellow  with  the  appearance 
cheese,  but  more  granular.    A  dry  form  occurs  which  is  rounded, 


PATHOLOGIC    PROCESS]  S  77 

circumscribed,  and  often  encapsulated,  and  never  Larger  than  a 
hazelnut. 

The  moist  form  is  softer,  paler,  and  li^s  sharply  circumscribed. 

Microscopically.-  Pine  granules  of  proteiu  material,  with  fatty 
debris,  arc  seen,  the  latter  in  advanced  cases  showing-  fatty  acid 
and  cholesterin  crystals,  and  sometimes  leucin  and  tyrosin.  The 
cells  can  uol  be  recognized,  at  least  in  fully  developed  cases, 
except  sonic  of  the  leucocytes. 

Results. —  Areas  may  persist  a  long  time  without  undergoing 
change  or  absorption  (possibly  due  to  destruction  of  autolysis  by 


SKI"**. 


Fig.    IS. — Large    tubercle    of    the    lung,    showing    cheesy    necrosis.       (Stengel    and    Fox.) 

toxins);  the  leucocytes  do  not  enter  the  area  (lack  of  cheniotac- 
tic  substances). 

Finally  calcification  occurs,  or  cysts  form  which  may  persist, 
or  be  absorbed  with  cicatrization. 

Fat  Necrosis 

Fat  necrosis  is  a  form  of  necrosis  occurring  in  fatty  tissues 
and  apparently  due  to  the  action  of  pancreatic  juice. 

Etiology. — It  is  believed  that  trypsin  injures  the  cells,  and 
the  lipase  (steapsin)  splits  the  fat  into  fatty  acids  and  glycerin, 
the  latter  being  absorbed  (and  may  appear  in  the  urine)  while 
the  acids  later  unite  with  calcium  to  form  insoluble  soaps. 


78  GENERAL   PATHOLOGY 

Any  condition  permitting  escape  of  pancreatic  juice  from  its 
normal  channels,  as  obstruction  of  the  duct,  acute  pancreatitis, 
tumors,  etc.,  may  act  as  a  cause. 

Locations. — This  necrosis  is  seen  in  abdominal  walls,  the  fat  in 
and  around  the  pancreas,  etc. 

Gross  Pathology. — The  areas  are  white  or  yellowish,  circum- 
scribed, varying  from  the  size  of  a  pinhead  to  a  pea,  may  be  soft 


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Fig.    16. — Focal    necrosis   in    the    liver    in   pneumonia.      (Delafield   and    Prudden.) 

or  gritty,  and  may  or  may  not  be  surrounded  by  an  inflammatory 
border. 

Microscopically.— Usually  but  little  of  the  original  structure 
remains.  The  necrotic  debris  consists  chiefly  of  calcium  soaps, 
crystals  of  fatty  acids,  etc. 

Results. — While  the  necrotic  areas  themselves  are  not  danger- 
ous to  life,  the  causal  conditions  are  usually  fatal.  When  re- 
covery does  take  place,  the  necrotic  foci  disappear  quickly. 

Focal  Necrosis 

Small  areas  of  necrosis  (microscopic  in  size  or  sometimes  visi- 
ble to  naked  eye)  are  often  found  in  the  liver,  less  often  in  the 


i ■  a'i  i ii ii ,< i. , i« •   p[;o('i:ssi:s  70 

kidney,  spleen  and  elsewhere,  in  eases  of  typhoid  fever,  less  often 
diphtheria,  septicemia  and  other  infections,  and  presumably  due 
to  toxins.     (  Fig.  16.) 

Gangrene 

Gangrene  has  been  defined  as  (1)  death  of  a  considerable  mass 
of  tissue,  which  may  become  dried  (dry  gangrene,  or  mummifica- 
tion) or  may  putrefy  (moist  gangrene)  due  to  saprophytic  inva- 
sion, or  (2)  and  probably  more  correctly,  as  putrefaction  of  ne- 
crotic areas. 

Primary  gangrene  is  that  due  directly  to  bacterial  invasion,  as 
in  malignant  edema,  and  hospital  gangrene. 

Secondary  gangrene  is  necrosis  subsequently  invaded  by  bac- 
teria. 

Etiology. — The  various  causes  as  given  under  necrosis  apply 
here.  Putrefactive  bacteria  are  said  to  be  present  in  all  cases, 
but  as  the  fluid  evaporates  from  the  part,  as  in  superficial  tissues, 
bacterial  action  becomes  less  and  less  conspicuous,  and  finally, 
in  complete  mummification,  ceases. 

Dry  gangrene  is  of tenest  caused  by  arterial  obstruction ;  freez- 
ing may  block  the  vessels  with  thrombi;  ergotism  and  Raynaud's 
disease  may  contract  the  vessels  and  shut  off  the  blood  supply; 
senile  gangrene  is  due  to  arteriosclerosis  with  enfeebled  heart 
action.  Dry  gangrene  may  also  follow  moist  gangrene  when 
putrefaction  is  slow  and  evaporation  marked.     (Fig.  17.) 

Moist  gangrene  is  usually  due  to  venous  obstruction,  but  may 
follow  any  circulatory  obstruction  or  destructive  agency:  (a) 
Strangulation  of  a  part — bowel,  appendix,  torsion  of  spleen,  kid- 
ney, tumor,  etc.  (b)  Internal  emboli  as  in  pulmonary  arteries 
and  veins,  or  mesenteric  arteries,  (c)  In  the  lungs,  it  may  fol- 
low pneumonia,  abscess,  bronchiectasis,  tumors,  and  diabetes. 
(d)  In  extremities,  it  may  follow  trauma,  diabetes,  physical 
agencies,  etc.  (e)  In  mucous  membranes,  it  may  follow  the  ac- 
tion of  toxins,  as  in  noma  of  the  mouth  or  genitals,  (f)  In 
cystitis,  it  may  follow  trophic  disturbances,  (g)  In  decubitus,  it 
is  due  to  trophic  and  circulatory  disturbances  combined. 

Locations. — Any  part  may  be  affected,  but  particularly  the 
distal  ends  of  upper  and  lower  limbs,  bowels,  lungs,  etc. 


80 


GENERAL    PATHOLOGY 


Gross  Pathology. — Gangrene  is  a  dark  greenish  or  black  (some- 
times "white"  or  anemic,  especially  in  early  stages)  area,  tem- 
perature is  below  normal,  the  area  is  usually  circumscribed,  and 
more  or  less  odorous.     The  part  is  separated  from  the  living  tis- 


Fig.     17. — Senile    dry    gangrene    of    the    lower    extremity,    showing    line    of    demarcation. 

(Hektoen.) 

sue  by  a  red  inflammatory  narrow  zone — -"the  line  of  demarca- 
tion. ' ' 

The  dry  form  has  the  following  distinctive  features:  The  part 
is  harder  and  the  surface  rough,  shrunken,  noncrepitant,  of  slight 
odor,  and  nearly  always  circumscribed.  The  line  of  demarcation 
advances  slowly. 

The  moist  form  has  the  following  distinctive  features:  Is 
softer  than  normal,  somewhat  swollen,  skin  covered  with  vesicles 


PATHOLOGIC    PROCESSES  81 

or  blebs,  and  discolored  fluids  ooze  from  sections  or  injured  parts. 
There  is  crepitation,  due  to  gases  of  decomposition.  The  line 
of  demarcation  advances  more  rapidly  than  in  the  dry  form. 
Occasionally  I  here  is  no  line  of  demarcation,  as  in  diabetes.  Oc- 
casionally there  arc  metastatic  forms  of  gangrene. 

Pathologic  Histology. — The  cells  have  become  converted  into 
granular  debris,  consisting  of  protein  matter,  fatly  granules, 
crystals  of  fatty  acids,  cholesterin,  leucin,  tyrosin,  phosphates, 
carbonates,  blood  pigments,  etc.  The  connective  tissue  and  elas- 
tic fibers  persist  longer  than  the  cells,  but  finally  become  lique- 
fied.   Bacteria  are  also  present. 

Results. — The  process  may  go  on  until  by  absorption  of  toxic 
products  death  ensues  (especially  true  of  the  moist  form,  due 
to  primary  invasion  of  bacteria,  or  to  disease  as  diabetes).  In 
other  cases  the  mass  is  cast  off  as  a  slough  or  sphacelus  at  the 
line  of  demarcation,  or  encysted  if  within  the  body,  followed 
by  resorption  and  calcification  or  cicatrization  of  the  gangrenous 
materials. 


CHAPTER  IV 

THE  CIRCULATORY  CHANGES 

The  circulatory  changes  are  usually  studied  under  the  follow- 
ing headings:  fa)  Ischemia,  or  Local  Anemia;  (b)  Hyperemia; 
(c)  Hemorrhage;  (d)  Thrombosis;  (e)  Embolism;  (f)  Infarcts; 
and   (g)   Edema. 

Ischemia,  or  Local  Anemia 

Ischemia,  or  local  anemia,  is  a  decrease  of  blood  in,  or  total 
absence  from,  some  part  of  the  body. 
Etiology. — According  to  cause  we  have — 

1.  Co'/i//ov//  anemia,  due  to  blood  having  passed  in  excess  to 
some  other  part,  as  cerebral  anemia  from  shock  or  fainting,  the 
blood  passing  to  the  dilated  abdominal  vessels. 

2.  Obstructive  anemia,  or  ischemia,  due  to  obstruction  of  the 
blood  supply  to  any  part,  as  anemic  infarct,  pressure  of  tumors, 
tight  bandage,  ligatures,  cicatrices,  obliterating  endarteritis, 
etc. 

3.  Neurotic  anemia,  due  to  (a)  stimulation  of  the  vasoconstric- 
1  ni-s  (neurotonic  anemia)  as  in  the  first  stage  of  Raynaud's  dis- 
ease, ergotism,  etc.,  or  to  (b)  paralysis  of  the  vasodilators  (neu- 
roparalytic anemia)  as  in  pallor  from  strong  emotions,  fright, 
anger,  etc. 

4.  Anemias  due  to  causes  acting  directly  on  the  vessels  and 
in  other  ways  not  fully  understood  (hence  the  "idiopathic  ane- 
mias" of  some  authors),  as  heat,  cold,  toxins,  etc. 

Gross  Morbid  Anatomy. — The  part  is  pale,  lower  in  tempera- 
ture, smaller  in  size,  less  in  weight,  and  more  or  less  bloodless 
on  section. 

Minute  Anatomy. — Blood  cells  are  abnormally  decreased  or  ab- 
sent from  the  vessels.  In  long  standing  cases,  atrophy,  degenera- 
tive and  necrotic  changes  may  be  noted. 

Pathologic  Physiology. — Function  is  unaffected  or  may  be  di- 
minished.    Occasionally  the  part  is  painful  or  tremulous. 

S2 


CIRCULATORY    CHANGES  83 

Results.-  -Mild  degrees  recover,  especially  if  treated.  In  cases 
due  to  blocking  of  the  vessel,  anastomotic  circulation  may  fully 
restore  the  part.  In  severe  and  prolonged  cases,  atrophy,  de- 
generative and  necrotic  changes  result. 

Hyperemia 

Hyperemia  is  excess  of  1)1  ood  in  a  part.  It  is  active  when 
excess  of  blood  is  brought  to  a  part  by  the  arterial  system;  pas- 
sive, when  the  normal  removal  of  blood  is  interfered  with  by 
the  venous  system. 

Active  Hyperemia 

Etiology. — According  to  cause  Ave  have — 

1.  Collateral  hyperemia,  due  to  anemia  in  another  part,  as 
around  anemic  areas,  or  by  bandaging  a  limb  preparatory  to 
amputation,  etc. 

2.  Increased  heart  action  may  cause  hyperemia,  though  proba- 
bly only  supplementary  to  other  causes  or  local  conditions. 

3.  Neurotic  hyperemia,  due  to  (a)  stimulation  of  vasodilators 
(neurotonic  hyperemia)  as  in  certain  forms  of  neuritis,  as  herpes 
zoster,  or  the  rash  of  teething  infants,  etc.,  also  in  erythro- 
melalgia  (red,  painful,  pulsating  areas  of  hands  and  feet)  blushing, 
etc.,  or  due  to  (b)  paralysis  of  vasoconstrictors  (neuroparalytic 
hyperemia)  as  in  hyperemia  of  a  side  of  the  face  from  pressure 
of  a  tumor  upon  the  cervical  sympathetic;  certain  forms  of 
migraine  may  also  belong  here. 

4.  Cases  due H^,, agencies  whose  action  is  imperfectly  under- 
stood, as  heat,  reaction  from  temporary  pressure,  certain  drugs, 
toxins,  increased  functional  demand,  etc. 

Gross  Anatomy. — The  part  is  red — color  disappearing  on  pres- 
sure, temperature  of  superficial  parts  somewhat  raised,  size  and 
weight  increased  (due  in  part  to  hypertrophy).  The  part  is 
bloody  on  section. 

Minute  Anatomy. — The  vessels  are  abnormally  filled  with  blood, 
occasionally  there  is  a  capillary  hemorrhage  into  the  tissues. 

Pathologic  Physiology. — Function  is  unaffected  or  increased 
when  hyperemia  is  moderate  and  uncomplicated.  In  tensely 
fdled  encapsulated  organs  the  function  may  be  impaired  from 
compression  of  the  parenchyma. 


84  GENERAL   PATHOLOGY 

Results. — Mild  cases  recover.  Mild  prolonged  cases  may  cause 
hypertrophy.  In  severe  and  prolonged  cases  capillary  hemor- 
rhage may  occur,  or  the  vessels  may  remain  weak  and  liable 
to  repeated  dilatation  from  slight  causes  or  be  followed  by  in- 
flammation. 

Passive  Hyperemia 

Etiology. — 1  General  causes  are  enfeebled  heart  action  from 
obstructive  heart  disease  or  from  any  cause ;  also  insufficient 
muscular  exercise,  disease  of  lungs  interfering  with  outflow  of 
blood  from  right  side  of  heart,  etc. 

2.  Local  causes,   as  pressure   on  veins  by  tumors,   aneurysm, 


& 


■     '", 


•    ■ ' , 


Id 


Fig.    18. — Chronic    passive    congestion    of    the    liver.       (Delafield    and    Prudden.) 

etc.,  or  interference  of  passage  of  blood  through  veins  as  parietal 
thrombi,  syphilitic  or  other  phlebitis,  etc. 

Gross  Anatomy. — The  part  or  organ  affected  is  dark  or  bluish 
(cyanotic),  the  color  disappearing  on  pressure.  The  brain  and 
cord,  however,  are  not  cyanotic  when  congested.  Size  and 
weight  are  increased,  temperature  of  superficial  parts  reduced. 
(Fig.  18.) 

Minute  Anatomy. — All  vessels  are  distended  with  blood. 
Edema  (excessive  lymph  within  tissues)  is  often  noted.  In 
prolonged  cases,  other  forms  of  degenerations  may  be  seen. 

Pathologic  Physiology. — Function  is  impaired.  The  part  or 
organ  is  at  first  painful,  later  anesthetic  (probably  pressure  on 
nerve  endings). 


CIRCULATOR'S    CH  \\<;i  s  85 

Results.  Mild  cases  may  recover,  but  tin'  process  is  more  ap1 
to  be  chronic  than  in  the  active  hyperemia.  Gradually  developed 
and  prolonged  cases  lead  to  atrophy,  degeneration,  edema,  pig- 
mentation or  cyanotic  induration  (fibrosis).  Severe  and  rapidly 
developed  cases  may  lead  to  coagulation  necrosis  and  gangrene. 

Hypostatic  Congestion 
Hypostatic  congestion  is  passive  congestion  or  hyperemia  oc- 
curring in  dependent  parts,  tine  to  enfeebled  heart  action.  It 
occurs  especially  in  debilitating  diseases,  in  low  fevers,  and  also 
commonly  just  prior  to  death  from  any  cause,  and  is  seen  usually 
in  the  skin  and  subcutaneous  tissues  of  back  and  buttocks,  and 
in  the  lungs. 

Hemorrhage 

Hemorrhage  is  the  escape  of  blood  from  blood  vessels. 
Type  I.  According  to  source  of  blood: 

(1)    Arterial   hemorrhage.      (2)    Venous.      (3)    Capillary.      (4; 
Mixed,  or  parenchymatous. 
Type  II.  According  to  mode  of  production: 

(1)  Hemorrhage  by  rhexis  or  laceration. 

(2)  Hemorrhage  by  diabrosis  or  ulceration,  caustic  action. 

(3)  Hemorrhage  by   diapedesis   or   oozing   of   blood   from   capil- 

laries or  venules  through  the  intercellular  cement  spaces 
("stomata")    and   due   to   increased   blood   pressure   or 
altered  vessel  walls. 
Type  III.  According  to  destination: 

(1)  External  Hemorrhages — upon  exterior  of  body  or  into  cavi- 

ties communicating  therewith,  as 
Epistaxis — hemorrhage  from  nose 
Hemoptysis  "  "      lungs. 

Hematomesis       "  "     stomach. 

Hematuria  "  "      urinary    tract. 

Enterorrhagia     "  "      intestines. 

Metrorrhagia      "  "      uterus  between  menses. 

Menorrhagia       "  "      uterus  during  menses. 

Hematidrosis       "  "      sweat  glands. 

(2)  Internal  Hemorrhages  into 
(a)  Closed  cavities,  as 

Hemothorax — hemorrhage  into  pleural  cavity. 
Hemoperitoneum      ' '  into  peritoneal   cavity. 

Hemoperieardium     ' '  into  into   pericardial   sac. 

Hematocele  "  into  tunica   vaginalis   testis 

or  other  small  cavity. 


86  GENERAL   PATHOLOGY 

(b)   Interstitial  or  Concealed  Hemorrhages,  as 

Ecchymosis — circumscribed  hemorrhage  beneath  skin  or 

mucous   membrane. 
Suffusion  of  Blood  or  Suggillation — diffuse  hemorrhage 

in  same  locations. 
Petechia? — minute   or    circumscribed   hemorrhage    (often 

punctiform). 
Hematoma — a  tumor-like  collection  of  blood. 
Hemorrhagic  Infarct — a  wedge  shaped  area  of  blood. 

Etiology. — (1)  Traumatism.  (2)  Erosion  by  surrounding  dis- 
ease, as  ulcer,  tuberculous  cavity,  etc.,  or  by  corrosion  of  caus- 
tics. (3)  Increased  blood  pressure,  as  in  great  excitement,  mus- 
cular effort,  increased  atmospheric  pressure  (caisson  disease), 
hypertropliied  heart  associated  with  arteriosclerosis,  etc.  (4) 
Alteration  of  vessel  walls,  resulting  from  degenerative  changes, 
as  in  aneurysm,  apoplexy,  cachexia?,  pressure  atrophy,  poisons, 
toxins  of  bacteria,  plants  or  snakes.  (5)  Nervous  influences: 
disease  or  section  of  the  cord,  apoplexy,  suppression  of  men- 
struation, etc.,  sometimes  cause  hemorrhage  from  other  parts,  as 
stomach,  nose,  etc. 

Gross  Anatomy. — The  blood  may  be  bright  red,  dark  or  black, 
according  to  length  of  time  retained  in  tissues  or  cavity.  In  in- 
terstitial hemorrhage  the  part  is  swollen. 

Microscopically,  the  tissue  is  infiltrated  with  blood  cells  or 
blood  pigment,  and  where  coagulation  has  occurred,  fibrin  may  be 
seen. 

Hemorrhage  is  checked  by:  (1)  Formation  of  clot  plugging 
the  bleeding  vessel.  In  certain  conditions,  especially  hemophilia 
(see  below)  the  blood  shows  little  or  no  tendency  to  clot.  (2) 
Reduction  of  blood  pressure.  (3)  Contraction  of  vessel  at  site 
of  hemorrhage  with  retraction  and  curling  up  of  the  middle  coat 
in  cases  in  which  arteries  are  cut  transversely.  The  contraction 
is  usually  followed  in  a  few  hours  by  relaxation,  which  may 
cause  secondary  hemorrhage.  (4)  Pressure  of  extravasated  blood 
upon  capillaries  in  interstitial  hemorrhages. 

Results. — Depending  upon  age,  health,  etc.,  about  y5  to  *4 
of  total  amount  of  blood  in  body  may  be  lost  without  fatal  re- 
sults. One  large  hemorrhage  is  more  apt  to  result  seriously  than 
a  larger  amount  of  blood  lost  in  small  and  oft  repeated  hemor- 
rhage.    The   total  amount  of  blood   (usually   given  as   %3)    is 


CIRCULATORY    CHANGES  87 

probably  only  '|i;  to  '  L.u  of  the  body  weight,  or  aboul  8  pounds 
for  average  adult. 

Blood  escaping  into  a  large  smooth  cavity  (as  pleural  or  peri- 
toneal) docs  not  clot  readily  and  may  be  wholly  or  in  large  part 
absorbed  by  lymphatics  and  returned  to  the  circulation. 

Hemophilia 

Hemophilia  is  a  condition  characterized  by  spontaneous  or 
readily  induced  homorrhages,  and  especially  by  delay  or  absence 
in  clot  formation  at  the  site  of  hemorrhage. 

It  is  usually  hereditary  though  acquired  cases  are  also  re- 
ported. Males  arc  much  more  frequently  affected  than  females 
(about  12  to  1),  but  the  diathesis  is  almost  exclusively  transmit- 
ted through  the  female  sex. 

Pathology. — Various  alterations  in  the  blood  have  been  ob- 
served, as  a  deficiency  in  calcium  salts,  in  blood  platelets  and  in 
prothrombin  but  these  changes  are  not  constant.  The  shed  blood 
in  many  cases  coagulates  as  rapidly  and  as  firmly  as  in  normal 
conditions.  The  occurrence  of  local  hemophilia  (where  vessels 
in  certain  regions  alone  show  this  tendency)  argues  against  gen- 
eral blood  changes.  It  is  probable  that  the  prothrombin  neces- 
sary for  fibrin  formation  at  site  of  hemorrhage  is  largely  fur- 
nished by  the  endothelial  cells  of  the  vessel  walls,  and  the  theory 
has  been  advanced  (Sahli)  that  these  cells  are  deficient  in  this 
particular  enzj'me  in  cases  of  hemophilia. 

Results. — Hemophiliacs  or  ''bleeders"  are  apt  to  succumb  to 
fatal  hemorrhage  during  the  early  years  of  life — the  later  the 
diathesis  manifests  itself,  the  more  favorable  the  prognosis. 
Secondary  anemia  is  usually  observed. 

Thrombosis 

Thrombosis  is  coagulation  of  blood  in  heart  or  blood  vessels 
during  life.  The  coagulum  is  called  a  thrombus.  Occasionally 
thrombi  of  fibrin  and  leucocytes  appear  in  the  lymph  vessels. 

Coagula  formed  postmortem,  or  those  formed  outside  of  the 
vessels  are  called  clots,  (this  distinction  is,  however,  not  main- 
tained by  all  writers). 

Types  of  thrombi: 


88  GENERAL    PATHOLOGY 

I.  According'  to  extenl  and  time  of  formation:  (1)  Primary 
thrombi  are  those  first  formed  and  confined  to  the  original  site. 
(2)  Propagated  thrombi — those  portions  subsequently  formed  and 
reaching  to  the  nearest  branch  of  the  vessel  or  further  (some  call 
these  "secondary").  (3)  Secondary  thrombi — those  formed  upon 
an  embolus  detached  from  a  primary  thrombus,  or  upon  a  pre- 
existing thrombus. 

II.  According  to  location:  (1)  Cardiac;  arterial;  venous,  in- 
cluding portal;  capillary;  and  lymphatic.  (2)  Proximal — those  on 
the  cardiac  side  of  a  causal  obstruction;  and  distal — those  on  the 
other  side  of  the  obstruction. 

III.  According  to  shape:  Parietal;  annular;  valvular;  ob- 
literative;  saddle  or  riding  (at  bifurcation  of  vessels);  polypoid 
or  pedunculated,  seen  usually  in  left  auricle;  ball  thrombi — de- 
tached pedunculated  forms. 

IV.  According  to  composition:  (1)  Red  or  currant  jelly  thrombi 
— rapidly  formed,  as  in  complete  stasis,  ligation,  and  death  (post- 
mortem clots),  and  containing  all  the  cellular  elements  of  the 
blood.  (2)  Yellow  or  chicken-fat  tlirombi — slowly  formed,  as  in 
prostrating  diseases,  or  in  slowly  approaching  death,  the  red 
cells  gravitating  to  the  lower  parts,  leaving  the  white  cells  on 
top.  The  chicken-fat  clot  is  formed  after  death  in  anemic,  espe- 
cially leucemic  diseases.  (3)  White  thrombi — consist  of  fibrin  with 
a  varying  number  of  leucocytes  and  of  platelets;  are  formed  in 
flowing  blood,  and  occur  in  heart  and  large  vessels,  as  peduncu- 
lated or  parietal  forms.  (4)  Stratified  thrombi — consist  of  alter- 
nating lamince  of  white  and  red  cells,  due  to  alternating  slowing 
and  accelerating  of  the  blood  current,  and  seen  in  dilated  vessels 
and  aneurysms.  (5)  Marantic  tlirombi  are  dark  colored,  composed 
almost  wholly  of  red  cells,  seen  in  dependent  vessels,  in  brain 
sinuses,  etc.,  and  in  the  lower  parts  of  chicken-fat  thrombi ;  they 
are  due  to  enfeebled  circulation  and  exhaustive  diseases,  maras- 
mus, etc.  Many  of  these  thrombi  have  been  found  to  be  in- 
fective. (6)  Agglutinative  or  hyaline  tlirombi  appear  to  be 
homogeneous  and  colorless;  usually  seen  in  plaque  thrombi,  which 
are  composed  of  blood  platelets  fused  together,  and  occurring  usu- 
ally in  the  heart  and  large  vessels:  also  in  conglutinative  thrombi, 
consisting  of  almost  colorless  red  blood  corpuscles  fused  together 
and  seen  in  diseases  attended  with  hemolysis;  as  anemias,  infec- 


CIRCULATOR'S    ('II  We  89 

tions,  poisons,  etc.  These  occur  usually  in  small  visceral  veins. 
(7)  Organized  thrombi — those  which  have  been  replaced  wholly  or 

in  part  by  new  connective  tissue.  (8)  Calcified  thrombi — found 
usually  in  veins,  as  phleholiths,  and  rarely  in  arteries  as  arte- 
rioliths,  and  in  hearl  as  cardioliths.  (9)  Canalized  thrombi  -those 
through  which  an  opening  has  been   formed  by  simple  softening 

(liquefaction  i rosis)  or  rarely  by  dilatation  of  a  longitudinally 

disposed  newly-formed  blood  vessel  in  an  organized  thrombus.  (10) 
Infectivi  thrombi — may  be  infective  from  the  start,  as  in  septic 
emboli,  or  may  be  subsequently  infected. 

Etiology. — (1)  Altered  cardiac  or  vessel  vails.  Any  agency 
which  roughens  the  intima  or  endocardium,  as  injury  in  ligation 
or  laceration,  pressure  of  tumors,  etc.,  or  disease  as  atheroma, 
local  inflammatory  or  degenerative  conditions,  or  action  of  para- 
sites, tissue  cells,  etc.  (2)  Altered  rate  of  blood  current.  Slow- 
ing favors  agglutination  of  leucocytes  and  platelets  to  cardiac 
and  vessel  vails  and  to  one  another.  Thrombosis  is  apt  to  occur 
in  sinuses  of  the  heart,  and  brain;  in  dilated  vessels,  aneurysms, 
etc.  (3)  Emboli.  (4)  Altered  blood.  Experimentally  the  in- 
jection of  tissue  extracts  (thymus,  suprarenals,  etc.)  containing 
fibrin  ferment:  of  hemolytic  agents,  as  nitrobenzol,  ether,  phenol, 
phytotoxins,  zootoxins,  and  bacterial  toxins  will  cause  thrombosis. 
Increase  of  calcium  salts,  hyperinosis  as  in  pregnancy,  etc.,  favor 
thrombosis. 

Gross  Anatomy. — Fresh  thrombi  are  jellydike,  moist  and  break 
with  a  gelatinous  fracture.  Old  thrombi  are  firm,  due  to  fibrosis 
or  calcification.     The  color  depends  upon  the  type. 

The  postmortem  clot  is  distinguished  from  a  thrombus  by  be- 
ing loose,  showing  no  evidence  of  attachment  to  heart  or  vessel; 
is  moist  and  shows  no  distinct  stratification,  though  in  slowly 
forming  clots,  the  upper  layer  may  be  paler  than  the  lower. 

Microscopically.—  -Freshly  formed  fibrin  presents  a  dense  net- 
work of  very  fine  fibrils,  with  "nodal  points"  or  granular  mat- 
ter at  the  points  of  intersection.  The  blood  cells  are  usually 
present  in  normal  proportion.  In  older  thrombi,  red  and  white 
cells  or  fibrin  predominate,  as  stated  under  the  various  types. 
In  organized  thrombi,  young  connective-tissue  cells  and  fibers, 
and  newly  formed  capillaries  are  seen,  the  elements  of  the  thrombi 


90  GENERAL    PATHOLOGY 

disappearing-  by  absorption.  "When  degenerative  processes  take 
place  the  evidence  of  such  is  observed. 

Results. — If  the  circulation  is  completely  stopped,  necrosis  of 
the  part  follows,  and  even  gangrene  when  putrefactive  organ- 
isms invade. 

Frequently,  however,  collateral  circulation  saves  the  part  from 
injury  in  which  event  the  thrombus  may  undergo  resolution,  or 
it  may  soften  so  rapidly  that  detached  portions  become  emboli. 
Again  thrombi  may  become  fragmented,  or  whole  thrombi  de- 
tached, thus  resulting  in  serious  embolism. 

Hyaline  degeneration  with  calcification  may  occur.  Organiza- 
tion will  often  displace  the  thrombus,  converting  the  vessel  into 
a  solid  fibrous  cord,  or  into  an  irregular  channel  with  fibrous 
trabecular,  the  latter  becoming  covered  with  endothelium. 

Embolism 

Embolism  is  the  transportation  and  lodgement  of  any  substance 
within  the  circulation,  capable  of  obstructing  the  flow  of  blood. 
Such  substance  (solid,  liquid  or  gas)  is  called  an  embolus. 

Types  of  Emboli : 

I.  According  to  location: 

1.  Cardiac  (rare)- — a  large  venous  thrombus,  detached  and 
doubling  upon  itself  may  occlude  the  pulmonary  orifice  in  the 
heart,  or  a  ball  thrombus  may  plug  the  valves. 

2.  Arterial — the  most  common  emboli  are  found  usually  in 
small  arteries  or  arterioles.  The  pulmonary  branches  are  the 
most  frequently  affected,  the  embolus  coming  from  a  thrombus 
in  the  right  side  of  heart,  or  venous  system.  Next  to  the  pul- 
monary arteries,  the  following  are  affected  in  order  of  frequency: 
arteries  of  kidney,  spleen,  cerebrum  (especially  the  middle  cere- 
bral) and  less  often,  or  at  least  less  often  detected,  in  lower  ex- 
tremities, upper  extremities,  liver,  stomach,  retina,  and  more 
rarely  elsewhere.  The  emboli  come  from  left  cardiac  and  aortic 
thrombi  or  atheromatous  ulcers,  and  rarely  from  the  right  side 
of  the  heart  or  venous  circulation  (paradoxical  emboli). 

3.  Capillary — usually  composed  of  tissue  cells,  bacterial  cells, 
oil  globules,  gases,  pigments  (malarial)  etc.  Various  metastases 
are  thus  explained. 


CIRCULATORY    CH  Wilis  01 

4.  Venous.  Since  veins  become  larger  in  the  direction  of  the 
blood  current,  embolism  occurs  in  the  systemic  veins  only  when 
the  venous  bloo<3  currenl  becomes  slowed  and  momentarily  and 
repeatedly  reversed,  or  when  ;i  foreign  body  by  its  own  weighl 
gravitates  againsl  the  blood  stream.  This  is  called  retrogressive 
embolism.  The  portal  vein  narrows  in  the  direction  of  the  blood 
stream  like  an  artery,  hence  emboli  from  the  spleen,  pancreas, 
gastrointestinal  tract  are  frequently  caugh.1  in  the  liver.  They 
are  often  infective. 

5.  Lymphatic — retrograde  embolism  occurs  as  in  veins  and  ex- 
plains certain  crises  of  metastasis  to  more  distal  points  as  can- 
cer of  humerus  from  axillary  "lands. 

G.  Paradoxical  or  crossed  embolism  occurs  when  emboli  orig- 
inating in  systemic  veins  or  right  auricle  find  their  way  to 
the  arterial  system.  They  pass  through  either  a  patulous  fora- 
men ovale  or  when  small  through  the  pulmonary  capillaries 
(which  are  larger  and  more  dilatable  than  the  systemic  capil- 
laries). 

II.  According  to  composition,  emboli  consist   of: 

1.  Fragments  of  thrombi — most  frequent  of  emboli — and  rarely 
whole  thrombi;  as  from  pelvic  veins. 

2.  Fragments  of  cardiac  A'alves  and  vegetations. 

3.  Calcareous  and  atheromatous  matter  from  atheromatous  ul- 
cers. 

4.  Tumor  cells  and  fragments  (neoplasmic  emboli)  which  have 
penetrated  the  vessel. 

5.  Tissue  cells,  as  from  liver,  placenta,  chorion  villi.  Lym- 
phocytes and  leucocytes  infiltrate  liver,  etc.,  in  myeloid  leueemia. 

6.  Parasites.  Animal  (as  filaria,  echinococcus,  etc.),  and  bac- 
terial emboli.  By  "septic  emboli"  is  usually  meant  those  in- 
fected with,  or  consisting  chiefly  of,  pyogenic  bacteria.  Pyemia 
is  thus  caused. 

7.  Extraneous  matter,  as  oil  globules  from  laceration  of  fatty 
tissue,  including  fractures  or  operations  on  long  bones;  pieces 
of  bone  in  comminuted  fractures;  bubbles  of  air,  as  may  happen 
when  veins  are  ruptured  or  cut  as  in  operations,  especially  about 
the  neck.  All  such  emboli  entering  vessels  through  injuries  are 
called  traumatic. 


GENERAL    PATHOLOGY 

Gaseous  emboli  may  also  occur  from  the  activity  of  aerogenic 

bacteria,  or  in  caisson  disease,  where  from  increased  atmospheric- 
pressure  gases  (chiefly  N)  may  accumulate,  and  expand  with  the 
formation  of  bubbles  on  reduction  of  pressure. 

Results  of  Embolism. — I  >cclusion  of  valvular  orifices,  pulmo- 
nary artery  or  one  of  its  main  branches,  one  of  the  coronary  ar- 
teries, or  a  large  cerebral  artery,  usually  causes  sudden  death. 

Iii  smaller  pulmonary  branches,  recovery  may  occur  after  a 
period  of  great  dyspnea.  When  many  small  branches  or  capil- 
laries are  plugged,  death  may  ensue:  fat  or  air  embolism  may  thus 
be  fatal.  It  is  also  thought  that  air  in  sufficient  quantity  can 
cause  death  by  forming  foam  which  interferes  with  the  heart's 
action. 

In  cases  of  small  emboli,  when  single  or  few  in  number,  col- 
lateral circulation  usually  relieves  the  part  from  degenerative 
change.  If.  however,  the  embolus  lodges  in  a  terminal  vessel. 
an  infarct  results. 

Thrombi  are  apt  to  form  upon  emboli.  If  an  embolus  should 
not  have  completely  occluded  a  vessel,  the  thrombus  will  stop 
the  floAv. 

Embolism  often  results  in  metastasis  of  malignant  tumors,  as 
sarcoma,  and  of  infections,  as  "embolic  abscesses'" — pyemic,  ame- 
bic, etc. 

Metastasis  means  the  transportation  of  living  material  from  a 
focus  of  disease,  capable  of  reproducing  the  disease  at  the  points 
of  deposit. 

Infarcts 

Infarcts  are  more  or  less  rone-shaped  necrotic  areas,  caused  by 
obstruction  of  the  terminal  or  "end  vessel"  of  a  part  (the  latter 
being  an  artery  having  no  collateral  branches  beyond  the  point 
where  it  breaks  into  capillaries  .  Occasionally  the  occlusion  of  a 
number  of  adjoining  arterioles  or  capillaries  causes  infarcts  of 
very  irregular  outline. 

The  essential  necrotic  change  in  infarcts  is  coagulation  nec- 
rosis, except  in  the  brain  where  liquefaction  necrosis  develops 
from  the  start. 

Two  forms  of  infarcts:  (A)  anemic  or  white,  which  are  de- 
void of  blood,  and  found  most  frequently  in  kidney,  spleen,  heart. 


CIRCULATOR'S    CH  ^NGES 


93 


brain,  stomach  and  intestine;  and  (B)  hemorrhagic  or  red,  which 
.,,,.  infiltrated  with  blood,  and  round  mosl  frequently  in  Lungs, 
less  often  in  spleen,  kidney,  and  other  Locations. 

Etiology.--  Embolus  or  thrombus  in  a  terminal  artery.  This. 
however,  is  not  necessarily  followed  by  infarction,  as  may  be 
seen  in  lungs  and  liver,  where  there  is  free  circulation.  Nor  need 
the  occlusions  always  be  in  a  terminal  artery— infarcts  may  occur 
m  intestines  with  free  anastomosis.  Again,  hemorrhagic  infarc- 
tion is  said  to  occur  by  occlusion  of  a  terminal  vein.  If  the  blood 
supply  be  too  slowly  occluded,  collateral  circulation  will  prevent 
infarction. 

The  manner  and  sequence  in  which  anemic  and  red  infarcts 
develop  have  occasioned  much  discussion.  Some  claim  that  the 
anemic  infarct  is  the  first  result  of  embolism,  the  red  infarct,  a 
secondary  condition.  Adami  believes  that  the  essential  factor 
in  formation  of  an  anemic  infarct  is  the  rapid  death  and  coagula- 
tion of  the  hemorrhage;  should  the  death  of  part  be  slowly  de- 
veloped, hemorrhage  is  permitted  to  occur  (red  infarct).  Why 
anemic  and  red  infarcts  may  be  found  at  different  times  in  the 
same  organ  depends  chiefly  on  the  condition  of  the  cells  at  the 
time,  for  experimental  ligation  of  the  renal  artery  is  followed  by 
necrobiosis  in  one  and  one-half  hours,  but  if  some  poison  (diph- 
theritic toxin-  he  previously  injected,  it  follows  in  three-quarters 

of  an  hour. 

Anemic  infarcts  develop  usually  in  dense  tissue,  as  kidney 
and  hemorrhagic  infarcts  in  loose  tissue,  as  lung;  this  has  thus 
been  explained:  the  capillaries  around  the  necrotic  area  become 
congested  (zone  of  hyperemia)  and  exude  serum  which  infiltrates 
the  "cells  in  the  immediate  vicinity,  causing  compression  of  the 
capillaries  and  prevent  the  progression  of  blood  into  the  necrotic 
area.  In  loose  tissue  the  capillaries  rupture,  infiltrating  the 
area  with  blood.  The  exceptional  cases  are  explained  by  path- 
ologic variations  in  looseness  or  density  of  the  tissues,  as  in  fatty 
degeneration  or  in  fibrosis  respectively. 

in  essential  factor  in  infarct  formation  is  smallness  of 
the  area  involved:  large  areas  suddenly  deprived  of  blood  be- 
come gangrenous.  A  possible  explanation  may  lie  in  the  fact, 
as  Weigert  claimed,  that  pervasion  of  an  area  with  blood  serum 


04 


GENERAL    PATHOLOGY 


is  necessary  for  coagulation  necrosis — large  areas  can  not  thus 
be  bathed  before  gangrene  has  set  in. 

Gross  Morbid  Anatomy. — An  anemic  infarct  is  a  cone-shaped 
or  irregular  whitish  or  yellowish  area,  softer  than  normal,  with 
apex  toward  occluding  vessel  and  base  toward  periphery,  its 
outer  surface  depressed  below  the  general  surface  of  the  organ. 
The  red  zone  of  hyperemia  can  usually  be  seen. 


Fig.   19. — Old  anemic  infarct  of  spleen.     C Stengel  and  Fox.) 

The  hemorrhagic  infarct  has  the  same  shape  and  location  as 
the  anemic,  but  is  red  or  dark  in  color,  firmer  than  normal,  and 
its  surface  elevated.  Subsequent  changes  will  alter  the  consist- 
ency in  both  forms. 

Microscopically. — In  the  anemic  form,  bloodless  areas  with  co- 
agulation necrosis,  fibrin  or  fibrinoid  material,  and  necrotic  cells 
are  seen.  Hemosiderin  is  sometimes  seen  and  rarely  hematoidin 
in  the  central  parts.  In  the  hemorrhagic  form,  blood  cells  with 
pigment  and  fibrin,  also  necrotic  tissue  cells  are  seen. 


CIRCULATOR'S    CHANGES  95 

The  occluding  embolus  or  thrombus  may  sometimes  lie  seen 
grossly  as  well  as  microscopically  in  sections  which  pass  through 
these  occluding  bodies. 

Results. — -(1)  The  area  may  become  encapsulated,  and  Ihe  con- 
tents undergo  fatty  change,  calcification,  caseation  or  liquefac- 
tion. 

It  may  be  gradually  absorbed  and  replaced  by  ingrowth  of 
fibrous  tissue,  which  subsequently  contracts,  forming  a  scar 
or  cicatrix. 

Infection  may  take  place  when  infarcts  are  so  located  as  to 
be  readily  reached  by  microorganisms,  as  in  lungs.  Those 
caused  by  infective  emboli  are  of  course  followed  or  associated 
with  infectious  processes.     (Fig.   19.) 

Edema,  Dropsy  or  Anasarca 

These  terms  signify  an  excess  of  fluid  in  the  tissues  or  body 
cavities.  The  term  edema  properly  applies  to  interstitial  infil- 
tration of  fluid  in  any  part;  anasarca,  to  widespread  subcuta- 
neous infiltrations:  wheals,  to  small  circumscribed  cutaneous  in- 
filtrations: drops)/,  to  fluids  in  cavities;  transudation,  to  fluid 
poured  out  in  noninflammatory  conditions ;  and  exudation,  to 
fluid  poured  out  in  inflammatory  processes. 

Etiology. — 1.  Increased  capillary  blood  pressure  due  to  pas- 
sive congestion,  pressure  upon  veins,  etc. 

2.  Increased  permeability  of  capillaries,  due  to: 

(a)  Alteration  of  blood,  containing  toxic  substance  as  in  in- 
fectious diseases,  Bright 's  disease,  anemias,  and  cachexias. 

(b)  Local  disease  of  walls,  as  in  inflammation. 

(c)  Nervous  influence,  as  in  paralysis  or  disease  of  brain  or 
cord,  in  neuralgia,  and  various  nervous  irritations.  This  may 
act  by  vasomotor  depression,  by  trophic  disturbance  of  intima, 
and  in  other  ways  not  understood. 

3.  Disturbed  osmotic  conditions.  The  tissue  fluids  may  be 
hypertonic  (contain  more  NaCl  than  the  blood)  causing  tran- 
sudation in  the  effort  to  establish  isotonicity.  Increased  NaCl 
content  of  the  affected  tissues  has  been  demonstrated  in  cardiac 
and  renal  dropsies. 

4.  Extensive  obstruction  of  lymphatic  vessels  will  prevent  the 
normal  removal  of  lymph,  as  in  chylous  ascites,  in  elephantiasis. 


96  GENERAL    PATHOLOGY 

etc.  In  moderate  obstruction,  the  venous  capillaries  can  remove 
all  the  lymph. 

5.  Decreased  pressure  in  tissue,  as  when  the  space  left  by 
atrophy  or  destruction  of  tissue  in  brain  or  cord  is  filled  with 
fluid  ("edema  ex  vacuo"). 

In  individual  cases  it  is  impossible  to  determine  how  many  of 
these  causal  factors  may  ho  associated,  or  in  some  cases  even  to 
name  the  chief  factors. 

We  have  the  following  types  of  edema: 

Cardiac — from  weak  heart  action  (passive  congestion)  seen 
in  dependent  parts,  as  ankles,  wrists,  hands,  bases  of  lung,  etc. 

Renal — from  nephritis  (seen  in  some  forms,  as  acute  nephri- 
tis), also  in  loose  tissue  (about  eyelids).  In  other  cases,  it  re- 
sembles cardiac  edema. 

Cachectic — seen  in  loose  tissue  about  eyelids,  backs  of  hands, 
etc.,  may  rarely  be  widespread.  This  is  seen  in  malignant 
diseases. 

Mechanical — due  to  venous  or  rarely  lymphatic  obstruction. 

Toxic — often  widespread  and  due  to  alterations  of  the  blood 
as  a  result  of  toxins. 

Angioneurotic — as  in  some  forms  of  urticaria,  due  to  vaso- 
motor disturbances. 

Lymphatic — often  widespread;  the  fluid  sometimes  is  milky 
in  appearance,  due  to  presence  of  fat,  mucoid  substance,  etc. 

Pulmonary  edema — so  called  when  the  air  cells  are  filled  with 
fluid. 

Chemosis — subconjunctival  edema. 

Dropsy  in  cavities  is  known  as: 

Hydrothorax,  Hydropericardium,  Hydroperitoneum  or  Ascites, 
Hydrocele  (in  tunica  vaginalis),  External  Hydrocephalus  (in 
cerebral  meningeal  sac),  Internal  Hydrocephalus  (in  cerebral 
ventricles),  External  Hyclrorrhachis  (in  spinal  meningeal  sac), 
Internal  Hyclrorrhachis  or  Syringomyelia  (in  central  spinal  ca- 
nal), Hydrops  Articuli   (dropsy  of  joints),  etc. 

Gross  Anatomy. — The  part  is  swollen,  tense  and  shiny  on  the 
surface,  pale,  pits  on  pressure,  has  a  doughy  consistence,  and 
subnormal  temperature  (deficient  circulation).  On  incision 
watery  fluid  escapes,  which  is  usually  clear,  thin,  pale  or  yel- 
lowish  (sometimes   red,   greenish   or   milky)  ;  contains  but  little 


CIRCULATOR!     CHANGES  97 

fibrinogen  and  albuminous  matter;  specific  gravity — 1.00s  to 
L.014.  [nflammatory  fluid  contains  more  albuminous  matter  and 
usually  coagulates  readily;  specific  gravity  1.018  to  1.020.  The 
tissue  infiltrated  is  firmer  than  normal. 

Microscopically.  I) r< 1 1 »sica I  fluid  may  sometimes  be  seen  in 
tissue,  appearing  homogeneous  and  electing  the  acid  stain.  In- 
flammatory edema  is  usually  granular  and  contains  ;i  certain 
amount  of  cellular  elements.  The  tissue  cells  are  separated  and 
may  be  hydropic  of  otherwise  degenerated. 

Result. — Acute  cases  recover  if  the  cause  can  be  removed. 
though  if  very  extensive  (as  in  pulmonary  edema)  or  in  unfa- 
vorable location  (as  in  edema  of  gdottis),  death  may  ensue. 

Where  the  condition  is  permanent  or  the  cause  can  not  be  re- 
moved various  forms  of  degenerations  and  fibrosis  result. 


CHAPTER  V 

INFLAMMATION 

Inflammation  is  a  compound  pathologic  process  represent- 
ing the  reaction  of  tissues  toward  an  irritant. 

Etiology. — Any  mechanical,  physical,  chemical,  infectious  or 
nervous  irritation,  sufficient  to  cause  local  injury,  but  insuffi- 
cient to  cause  immediate  extensive  necrosis. 

Perhaps  in  all  cases,  the  injured  (degenerated  or  necrosed) 
tissue  becomes  the  direct  irritant,  though  some  substances  as 
toxins,  etc.,  may  also  cause  emigration  of  leucocytes  by  their 
chemotactic  influence. 

Nervous  irritation  probably  acts  primarily  through  the  vaso- 
motor nerves. 

The  causes  may  be  divided  into  external  and  internal — the 
latter  being  products  of  abnormal  metabolism.  Again  we  have 
simple,  or  noninfective,  and  septic,  or  infective,  causes — the  es- 
sential difference  being  that  the  simple  are  not  reproductive, 
while  the  infective  are  constantly  being  reproduced  and  usually 
increased  until  the  reparative  processes  overcome  the  destruc- 
tive, or  death  ensues. 

Inflammation  is  either  acute — in  which  the  vascular  phenomena 
predominate;  or  chronic — in  which  the  proliferative  changes  pre- 
dominate. 

Gross  Pathology  of  Acute  Inflammation. — Heat,  redness,  pain, 
and  swelling  (calor,  rubor,  dolor,  tumor — of  Celsus)  are  the 
chief  general  characteristics.  (The  distinctive  features  of  the 
various  types  must  be  separately  described.) 

Microscopically,  the  following  histologic  changes  have  been 
noted :  The  arteries  and  arterioles  temporarily  contract,  but 
soon  begin  to  dilate,  and  in  "an  hour  or  so"  full  dilatation  of 
all  the  vessels  is  seen,  with  increased  blood  flow  (hyperemia). 
Gradually  the  blood  stream  becomes  slower,  the  corpuscles  leave 
the  central  axial  stream  (in  the  larger  vessels)  and  the  leucocytes 
adhere  to  the  vessel  walls  (marginatum) .     The  endothelium  be- 

98 


INFLAMMATION  !)!) 

(•(nut's  swollen  niid  probably  more  adhesive,  and  the  vessel  more 
permeable. 

The  (irst  elemenl  which  escapes  from  the  vessels  is  Hie  fluid 
of  the  blood  (a  transudation)  ;  Later  the  fluid  is  found  to  be  rich 
in  albuminous  substances  which  aid  in  proliferative  processes, 
and  this  modified  blood  plasma  villi  the  blood  cells  which  per- 
meate the  area  is  called  the  inflammatory  exudate.  The  leuco- 
cytes emigrate  before  the  red  blood  cells  pass  through  the  vessel 
walls  and  in  larger  numbers,  due  to  the  positive  chemotaxis  which 
attracts  them  to  the  irritant.  Red  blood  cells  always  pass  out  of 
the  vessels  into  the  affected  area  (diapedesis)  but  this  is  conspic- 
uous only  in  severe  grades  of  inflammation. 

The  leucocytes  are  chiefly  of  the  polymorphonuclear  (phago- 
cytic) variety,  but  in  some  cases  especially  in  inflammation  due 
to  animal  parasites,  eosinophils  are  also  found.  In  later  stages 
lymphocytes  abound,  derived  from  lymph  channels  and  from 
proliferation  of  local  lymphoid-tissue  cells.  Plasma  cells,  which 
arc  probably  altered  lymphocytes,  with  distinct  and  eccentrically 
placed  nuclei,  may  be  found  in  any  type  of  inflammation. 

Proliferation  of  the  fixed  connective-tissue  cells  and  the  endo- 
thelium of  lymph  spaces  and  capillaries  occurs  sooner  or  later, 
thus  forming  "round  cells"  with  large  pale  nuclei.  At  this 
stage  many  of  the  leucocytes  have  disappeared,  but  those  that 
remain  together  with  the  lymphocytes  and  proliferated  cells  just 
mentioned  constitute  the  so-called  "round-cell  infiltration." 
Some  of  the  newly  formed  connective-tissue  cells  become  "wan- 
dering cells"  which  are  more  or  less  phagocytic,  while  the  re- 
mainder elongate  and  form  fibrous  tissue  (fibroblasts). 

Degenerative  changes  are  always  present  in  varying  degrees,  con- 
sisting of  cloudy  swelling,  mucoid  or  fatty  degeneration,  coagula- 
tion necrosis,  liquefaction  or  other  necrosis. 

A  typical,  acute  inflammation  is  therefore  characterized  by 

Hyperemia  of  the  affected  area, 

Exudation  of  serum  from  the  vessels, 

Emigration  of  leucocytes, 

Diapedesis  of  red  blood  cells, 

Proliferative   changes  in  the   fixed  tissues, 

Degenerative  changes.     (Figs.  20,  21,  and  22.) 

There  are  ten  types  of  inflammation: 


100 


GENERAL    PATHOL* 


I.  Edematous  or  Serous. — In  this  type  there  is  an  excessive 
fluid  exudation,  with  little  tendency  to  fibrin  formation,  and 
relatively  few  cells,  due  to  intense  irritation.  -  steam  or  cor- 
rosives: or  to  mild  subacute  or  chronic  irritation,  as  in  serous 
effusions. 

II.  Fibrinous. — The  exudate  is  especially  rich  in  fibrin  factors, 
the  fibrin  appearing  as  fibrillar,   granular  or  homogeneous  de- 


Fig.     20. — Acute    inflammation.       (Mallory.) 


m 


■* 


% 


"^  f    f-OCA 

Fig.  21. — Inflammation  of  the  :  show- 

ing overfilling  of  the  blood  vessels,  with  emigra- 
tion of  let:  liapedesis  of  red  corpuscles. 
(Ziegler.) 


-  • 


<  Mallory.  > 


posits.  This  type  is  seen  most  typically  on  serous  surfaces,  but 
it  also  occurs  in  tissi 

III.  Diphtheritic  or  Croupous. — This  is  ntially  the  same  as 

the  fibrinous,  but  with  more  pronounced  coagulation  necrosis 
of  the  cellular  elements,  thus  forming  a  tough  membranous  pellicle 
— the  false  membrane.     This  type  is  met  with  most  typically  on 


[NFLAMMATION  I'll 

mucous  surfaces,  due  to  bacteria  (as  the  diphtheritic  bacilli,  strep- 
tococci, etc.)j  steam,  chemicals,  etc.     I  Pig.  '23.) 

IV.  Suppurative. — Characterized  by  excess  of  leucocytes  and 
liquefaction  of  the  exudate  and  fixed  tissues.  Clinically  prob- 
ably always  due  to  pyogenic  organisms  (usually  pyococci,  less 
often  pneumococci,  colon  and  typhoid  bacilli,  and  other  organ- 
isms) bul  injections  of  sterilized  cultures,  toxins,  croton  oil,  tur- 
pentine, calomel,   iodoform,  etc.,   can   also   cause  pus  formation. 

The  irritant  being  strongly  ehemotactic  accounts  for  the  ex- 
ive   local    leucocytosis.     Enzymes   liberated    from   the    leuco- 


ranous  inflammation   of  the  uvula:     a.  a,  masses  of  micrococci;   b,  b, 
necrotic    cells;    c,    c,    round-cell    infiltration;    d,    d,    fibrin    network.      (Ziegler.) 

cytes  and  probably  other  cells,  and  perhaps  also  in  part  by  the 
bacteria,  prevent  fibrin  formation,  or  liquefy  what  does  form, 
together  with  the  exudate  and  tissue,  thus  forming-  pus. 

Pus,  is  a  yellowish,  thick,  usually  alkaline  (specific  gravity 
1.020  to  1.040)  fluid,  containing  pus  cells  in  suspension.  Pus 
cells  consist  chiefly  of  polymorphonuclear  leucocytes,  also  a 
small  number  of  proliferated  connective-tissue  and  endothelial 
cells,  all  more  or  less  degenerated  (typically  cloudy,  swollen, 
clearing  on  adding  acetic  acid)  or  necrotic  (shown  by  karyoly- 
sis,  etc.)  Pus  may  contain  as  many  as  1.000,000  cells  per  c.mm.; 
1  oz.  (30  c.c.)  would  thus  contain  nearly  as  many  leucocytes  as 
does  the  total  amount  of  blood,  illustrating  the  enormous  cell 
reproductive  power  of  the  body  tissues. 


K'2  GENERAL   PATHOLOGY 

The  fluid  (liquor  puris)  contains  proteins  normal  to  blood,  as 
well  as  derived  proteins,  albumoses,  peptones,  etc.,  also  shreds 
of  muscles,  fibrous  or  elastic  tissue  variously  degenerated,  blood 
pigment,  sometimes  bacterial  pigment,  fatly  acid  crystals,  cho- 
lesterin,  etc.  Bacteria  may  be  present,  free  in  the  fluid  or  with- 
in the  cells;  frequently,  however,  the  bacteria  are  destroyed  by 
products  of  their  own  manufacture,  or  by  action  of  the  cells  and 
exuded  fluids.  Such  pus.  as  well  as  thai  caused  to  form  by 
noninfective  agents,  is  called  "sterile  pus." 

Suppuration  may  occur: 

Within  tissues,  as  a  circumscribed  collection  of  pus  (abscess) 
or  as  a  diffuse  infiltration  (purulent  infiltration  or  phlegmonous 
inflammation). 

On  free  surfaces,  with  considerable  loss  of  tissue  (ulcer). 

On  serous  surfaces  or  in  serous  cavities  as  an  empyema. 

On  mucous  surfaces,  as  purulent  catarrh,  pyosalpinx,  etc. 

Abscess  Formation. — When  a  suppurative  inflammatory  area 
first  liquefies  in  the  center  (which  it  does  usually  in  forty-fin  lit 
hours)  an  abscess  is  formed,  i.  e.,  a  cavity  filled  with  pus  sur- 
rounded with  a  wall  of  inflammatory  tissue,  rich  in  leucocytes. 
The  abscess  grows  by  liquefaction  progressing  from  within  out- 
ward, the  inflammatory  wall  growing  with  equal  pace.  After 
sufficient  time  (four  to  ten  days)  granulation  tissue  (see  Repair) 
forms. 

A  fully  developed  abscess  wall  therefore  consists  of  an  inner 
zone  composed  largely  of  leucocytes,  exudate  and  intercellular 
matter  about  to  liquefy;  next  a  zone  of  inflammatory  exudate 
with  its  granulations  projecting  into  the  preceding,  and  of  con- 
gested capillaries  (the  source  of  leucocytes)  hence  called  "pyo- 
genic zone,"  (formerly  "pyogenic  membrane").  The  outer 
part  of  this  zone,  being  the  youngesl  part  of  the  wall,  usually 
shows  more  fibroblasts  and  mitotic  figures  than  the  middle  por- 
tion. 

Results. — The  abscess  travels  in  the  direction  of  least  resist- 
ance (called  "pointing")  which  is  usually  tOAvard  the  surface  of 
an  organ  or  part,  because  the  pressure  is  less  on  that  side  and 
because  there  is  greater  vascularity  on  its  inner  side,  hence 
more  leucocytes  and  resistance. 


[NFL  v.m  \i  \ti<>\  103 

Rupture  or  incision  of  an  abscess  relieves  tension  and  causes 
the  fluid  exudate  in  the  abscess  wall  to  flow  toward  and  into  the 
cavity,  flushing  out  the  tissue  spaces  of  bacteria  and  toxic  prod- 
ucts, and  favoring  protective  (phagocytic,  bacteriolytic  and 
probably  antitoxic)   and  reparative  processes. 

In  small  abscesses  or  pustules,  complete  restitution  may  oc- 
cur; in  Larger  ones,  cicatrization  follows  healing  (see  Repair). 
Sometimes  encapsulation,  with  inspissation  or  calcification,  oc- 
curs. 

Death  may  ensue  from  intoxication  when  abscesses  are  very 
Large  or  multiple,  or  when  vital  organs  are  involved,  or  when 
rupture  occurs  into  large  vessels,  peritoneum,  etc. 

In  acute  bacterial  action,  stasis  is  apt  to  occur  in  the  vessels 
of  affected  areas  (thrombosis  and  thrombophlebitis)  thus  prevent- 
ing hemorrhage  even  when  eroded;  but  bacteria  are  also  liable 
to  grow  into  and  through  these  plugged  vessels  and  constitute 
one  of  the  ways  in  which  metastasis  occurs. 

Special  forms  of  abscesses : 

A  Furuncle  (boil)  is  a  subcutaneous  abscess,  beginning  in  a 
sweat  gland,  sebaceous  gland,  or  hair  follicle. 

A  Carbuncle  is  a  similar  but  more  extensive  abscess,  beginning 
in  several  glands  or  follicles  simultaneously.  Its  favorite  seat  is 
in  the  back. 

A  Pustule  is  a  term  properly  applied  to  a  suppurat'.ig  vesicle, 
though  often  applied  to  any  minute  superficial  absce  ,s. 

Pyemia  is  a  condition  in  which  multiple  abscesses  e-  ist  through- 
out the  body,  due  to  emboli  of  pyogenic  bacteria. 

An  acute  abscess  is  often  called  a  "hot  abscess,"  in  contrast  to 
the  so-called  "cold  abscess,"  a  term  practically  limited  to  lique- 
faction of  tuberculous  bone  disease,  as  in  lumbar  vertebra?. 

Phlegmonous  Inflammation. — This  is  a  spre  ding  inflamma- 
tion  with  a  tendency  to  suppuration.  In  these  <  ises  "wall  build- 
ing" characteristic  of  abscess  is  inadequate;  tl  i  bacteria  are  not 
confined,  the  process  spreads  more  or  less  ra  idly,  and  metasta- 
sis is  apt  to  occur  through  lymph  and  bloc  .  vessels.  It  is  al- 
ways serious  and  sometimes  attended  with  xteusive  loss  of  su- 
perficial tissue. 


104 


GENERAL    PATHOLOGY 


An  Ulcer  is  an  area  of  superficial  suppuration  with  erosion  of 
the  skin  or  mucous  membrane.  The  floor  of  the  ulcer  is  similar 
histologically  to  an  abscess  wall.     Ulcers  may  be  divided  into: 

Phagedenic — rapidly   spreading   and   destructive. 

Serpiginous — snake-like  and  irregular,  healing  on  one  side  and 
progressing  on  another. 

Fungous — in   which   excessive   granulation   tissue   forms. 

Indolent — in  which  granulation  tissue  is  slow  in  forming. 

Gangrenous — in  which  putrefaction  is  an  added  feature. 

Follicular — small  in  extent  as  in  crypts  or  follicles  of  glands. 


Fig.    24. — Tuberculous    ulceration    of    the    intestine.      fStengel    and    Fox.) 

Specific — due  to  tuberculous,  syphilitic  or  other  infection. 
(Fig.  24. 

Peptic — due  primarily  to  the  digestive  action  of  enzymes. 

V.  Catarrhal  Inflammation  is  inflammation  of  a  mucous  mem- 
brane, characterized  by  degeneration  of  epithelium  (mucoid, 
fatty  or  necrotic)  which  is  discharged  with  the  abundant  serous 
exudate  upon  the  surface.  The  submucous  tissue  is  infiltrated 
with  a  more  or  less  serous  exudate.     (See  Fig.  25.) 

AVhen  there  are  abundant  leucocytes  we  have  a  purulent  or 
mucopurulent  catarrh. 

In  chronic  forms,  productive  processes  lead  to  overgrowth  of 
connective  tissue,  giving  an  appearance  of  hypertrophy  of  the 
mucosa.  Later 'on.  contraction  of  the  fibrous  tissue  causes  atro- 
phy. 


IM'I.AMM  ATIOX 


105 


Follicular  Inflammation  are  terms  applied  to  swollen  lymph 
follicles,  or  in  mucous  glands  (from  obstructed  duets;  the  resull 
of  inflammation. 

VI.  Parenchymatous  Inflammation  are  terms  used  when  the 
degenerative  changes  occurring  in  the  parenchyma  Tor  function- 

- 


Fig.    2: 


-Acute  bronchial   catarrh,   showing  the   escape   of   leucocytes   from  the   submucous 
tissue  between  the  epithelial  lining  cells.      (Thoma.) 


r 


Fig.  26. — Chronic  interstitial  nephritis:  great  increase  of  connective  tissue  around 
the  glomeruli,  renal  tubules,  and  blood-vessels;  from  a  case  of  arteriocapillary  fibrosis. 
I  Stengel  and   Fox.) 


106  GENERAL   PATHOLOGY 

ating  cells)  of  an  organ  are  more  conspicuous  than  the  inflamma- 
tory changes  in  the  interstitial  tissues. 

VII.  Interstitial  Inflammation. — Strictly  speaking,  inflamma- 
tion proper  occurs  only  in  interstitial  tissue,  but  the  term  is  ap- 
plied to  more  or  less  chronic  inflammation  of  an  organ,  attended 
by  decided  overgrowth  of  fibrous  tissue.  (Fig.  26.) 

VIII.  Hemorrhagic  Inflammation  occurs  when  the  diapedesis 
of  red  blood  corpuscles  is  excessive,  due  to  intense  irritation. 

IX.  Necrotic  or  Gangrenous  Inflammation  occurs  when  irrita- 
tion is  intense  or  the  body  resistance  is  low,  as  cancrum  oris. 

X.  Productive  Inflammation — when  proliferative  changes  pre- 
dominate over  the  degenerative  and  other  changes.  Two  types 
of  productive  inflammation  may  be  considered: 

(1)  When  the  framework  of  organs  or  tissues  is  especially 
proliferated,  we  have  interstitial  inflammation  (see  Type  VII). 

(2)  When  loss  of  tissue  is  being  replaced  we  have  the  phenom- 
ena occurring  in  repair  of  wounds,  healing  of  abscess  or  ulcer, 
organization,  etc.  (A)  Repair  of  Wounds.- — (a)  Healing  by 
Immediate  Union :  When  the  margins  of  a  very  slight,  clean 
wound  are  closely  apposed,  there  is  a  minimum  of  capillary 
hemorrhage,  the  coagulation  of  which  cements  the  margins  of 
the  wound  together,  holding  them  firmly  so  that  repair  work 
may  proceed,  which  consists  of  a  minimum  of  exudation,  emigra- 
tion of  leucocytes  and  cellular  proliferation;  the  dead  cells  are 
removed  by  phagocytosis,  liquefaction  and  absorption;  the  tissue 
cells  and  epithelial  cells  undergo  division  until  the  space  is 
bridged  over;  the  capillaries  throw  out  bud-like  processes  from 
both  sides  which  unite  across  the  gap ;  there  are  no  new  vessels 
formed,  and  no  scar  tissue  produced. 

(b)  Healing  by  First  Intention:  In  larger  aseptic  wounds, 
the  margins  of  which  are  more  or  less  separated,  and  the  gap 
filled  with  coagulated  blood,  the  healing  processes  are  the  same 
as  in  (a),  but  there  is  greater  inflammatory  reaction  and  more 
cellular  proliferation.  New  blood  vessels  are  formed  and  fibrous 
tissue  formation  with  cicatrization  (scar  formation)  occurs. 

(c)  Healing  by  Second  Intention:  This  occurs  when  the  gap 
between  the  margins  is  not  filled  with  blood  or  exudate,  and  the 
margins  are  not  approximated,  or  when  the  filled  gap  becomes 
infected  and  pus  separates  the  margins,  or  when,  as  in  an  ulcer, 


tNFLAM  \l  V.TION 


107 


there  is  loss  of  surface  tissue.  Here  new  capillaries  form  to  sup- 
ply nutrimenl  for  the  extensively  proliferating  processes;  then 
endothelial  cells  become  swollen  and  scud  ou1  solid  protoplasmic 
processes,  which  unite  with  similar  processes  from  the  same  or 
neighboring  capillaries,  thus  forming  loops  which  become  cen- 
trally perforated  to  carry  the  Mood;  these  loops  as  they  project 
into  the  area  of  injury,  covered  with  proliferated  tissue  cells, 
look  like  granules,  hence  the  tissue  is  called  "granulation  tissue." 
This  forms  until  all  the  lost  tissue  has  been  replaced.  Contrac- 
tion of  the  fibrous  tissue  results  in  a  scar  of  greater  or  lesser 
extent.     (Figs.  27  and  28.) 

(d)    When  two  granulating  surfaces  meet,  as  is  well  shown  in 


a,  no'tfyivAi 


Fig.    27. — L,oops   of   blood-vessels    in    granu- 
lation   tissue.      (Thiersch.) 


Fig.  28. — Formation  of  new  blood-vessels  as 
seen  in  the  tail  of  a  tadpole.     (Arnold.) 


opposite  walls  of  an  abscess,  or  large  gaping  wound,  the  process 
is  sometimes  called  "healing  by  third  intention." 

(B)  Adhesions  between  serous  surfaces,  organization  of 
thrombi  or  other  dead  areas,  healing  through  fragments  of  bone, 
ivory  or  sponge  (''healing  upon  a  scaffold")  are  all  processes 
similar  essentially  to  healing  by  first  intention.  The  foreign 
body  may  be  softened  and  absorbed,  or  encapsuled  (surrounded 
by  dense  fibrous  tissue). 

When  repair  processes  are  relatively  extensive  or  prolonged, 
giant  cells — "the  giant  cells  of  repair"  are  found.     They  origi- 


10S  GENERAL   PATHOLOGY 

nate  either  by  division  of  nuclei  without  division  of  cytoplasm, 
or  by  confluence  of  cells.    Many  of  them  are  phagocytic. 

Repair  of  a  slight  wound  in  avascular  tissues,  as  the  cornea, 
may  occur  directly  by  proliferation  of  the  lost  cells,  without 
the  essential  phenomena  of  inflammation. 

Regeneration 

Regeneration  is  the  formation  of  new  tissue  to  replace  that 
which  has  been  lost. 

Physiologic  regeneration  occurs  constantly  either  to  counter- 
balance the  loss  from  wear  and  tear,  or  to  form  new  cells  (in  ex- 
cess of  those  destroyed)  in  the  process  of  growth. 

Pathologic  regeneration  is  often  atypical  and  usually  exces- 
sive.    The  etiology  is  not  known.     The  cells  have  an  inherent 


Fig.    29. — Fibroblasts    forming    fibrous    tissue.       (Ziegler.) 

tendency  to  multiply,  with  some  restraining  influence.  In  dis- 
ease there  may  be  stimulation  of  reproduction  by  toxic  products 
or  other  agencies,  and  a  reduction  of  restraint  by  removal  of  pres- 
sure, etc. 

Pathologic  Anatomy. — The  cells  swell,  and  multiply  by  mito- 
sis, or  rarely  by  amitosis.  The  latter  is  supposed  to  be  "a  ret- 
rograde process  in  every  instance."  The  cells  subsequently 
form  their  characteristic  intercellular  substance. 

The  less  specialized  a  tissue  may  be  and  the  younger  the  or- 
ganism, the  more  capable  it  is  of  regeneration,  e.g.,  the  connec- 
tive tissue  of  an  organ  will  always  outstrip  the  parenchyma,  if 
the  latter  regenerates  at  all. 

Pathologic  Regeneration. — In  connective  tissue,  the  cells  swell 
and  multiply  by  mitosis.  The  new  cells  are  round  or  oval  with 
paler  nuclei  than  normal,  and  occur  in  great  numbers ;  hence  the 
tissue  is  said  to  have  reverted  to  the  embryonal  type.     The  cells 


INFLAMMATION 


1  09 


form  intercellular  substance  or  fibrils  (i.e.,  they  arc  "fibro- 
blasts") and  later  elongate  and  become  relatively  less  numer- 
ous, as  well  as  decreased  in  size  The  polymorphonuclear  leu- 
cocytes which  infiltrate  inflammatory  areas,  do  not  become  con- 
verted into  connective-tissue  cells,  and  whether  other  types  of  leu- 
cocytes and  endothelial  cells  do,  is  undetermined,  though  the 
budding  processes  of  endothelial  cells  in  the  formation  of  new 
blood  vessels  seem  to  indicate  the  possibility  of  such  conversion. 
I  Fig.  20.) 
Epithelial  cells  are  regenerated  by  mitosis,  and  usually  in  ex- 


i 


.«<■        ■     «k>  4.1'fi  &•>*  *£  V  t      '  ' 

-.    -  -  ■>'   - ','  ^ 


Fig.   30. — Regeneration  of  epithelium.      (Delafield  and  Prudden.) 

cess  of  those  lost — the  surplus  being  later  degenerated  and  ab- 
sorbed.    (Fig.  30.) 

Striated  muscle  cells  regenerate  to  some  extent,  but  rarely 
completely  so.  The  destroyed  area  is  first  replaced  by  connec- 
tive tissue,  into  which  the  new  muscle  fibers  grow. 

Smooth  muscle  fibers  are  probably  never  regenerated. 

Nerve  fibers  regenerate,  but  highly  specialized  cells  as  the 
multipolar  cells  of  the  cord  do  not. 

Fatty  tissue  begins  with  the  formation  of  fat-free  cellular  tis- 
sue— later  the  cells  become  infiltrated  with  fat. 

Elastic  tissue  is  capable  of  regeneration. 


110  GENERAL    PATHOLOGY 

Cartilage  may  be  regenerated,  beginning  from  the  perichon- 
drium, the  proliferated  cells  of  which  (chondroblasts)  are  at  first 
indistinguishable  from  fibroblasts.  Fibrillar  tissue  first  forms, 
which  is  later  removed  or  becomes  transparenl  and  hyaline,  thus 
forming  cartilage.  To  a  certain  extent,  the  original  cartilage 
cells  near  the  line  of  injury  also  proliferate.  "Very  commonly, 
however,  regeneration  of  fractures  of  cartilage  is  mainly  fi- 
brous. ' ' 

Bone  is  also  regenerated  from  the  periosteum,  the  proliferated 
cells  being  indistinguishable  from  fibroblasts ;  fibrous  tissue 
forms,  which  later  is  infiltrated  with  lime  salts  (the  cells  now 
being  called  osteoblasts).  Essentially  the  same  process  takes 
place  from  the  marrow.  The  infiltrated  tissue  forms  the  callus 
or  splint  which  holds  the  margins  of  fractured  bones  together, 
until  the  true  osseous  tissue  is  formed. 

Glandular  tissue  is  but  imperfectly  regenerated,  or  not  at  all. 

Metaplasia  is  the  direct  conversion  of  one  form  of  tissue  into 
another,  as  when  connective  tissue  becomes  cartilage,  bone  or 
mucoid  tissue ;  or  when  epithelium  changes  from  the  columnar 
form  to  the  squamous,  as  in  covering  of  a  healing  ulcer  in  the 
trachea.  Metaplasia  is  true  only  of  tissues  of  the  same  type, 
e.g.,  epithelium  can  never  become  connective. 

Heteroplasia  means  production  of  a  tissue  within  a  part  to 
which  it  is  foreign,  as  when  cartilage  or  bone  forms  in  the  pa- 
rotid gland,  ovary  or  testicle.  It  is  really  metaplasia,  since  it  is 
the  connective  tissue  of  the  part  which  is  converted  into  bone, 
etc. 


CHAPTER  VI 

PROGRESSIVE  TISSUE  CHANGES 
Hypertrophy 

Hypertrophy  is  a  simple  progressive  process,  resulting  in  ab- 
normal increase  of  a  part  or  organ.    There  are  two  types : 

(a)  Simple  hypertrophy  is  an  increase  in  the  size  of  the  cells. 

(b)  Numerical  hypertrophy  or  hyperplasia  is  an  increase  in 
number  of  the  cells. 

Both  types  are  usually  found  associated  (combined  hyper- 
trophy). 

True  hypertrophy  is  increase  in  size  of  all  the  tissues  of  which 
a  part  is  composed,  and  the  relationship  of  the  parts  is  not  ma- 
terially altered,  as  in  hypertrophy  of  heart,  uterus,  etc. 

False  hypertrophy  or  hyperplasia  occurs,  when  one  or  other 
of  the  constituent  tissues  is  alone  increased,  or  in  excess  of  the 
other  parts.  Examples  are  cirrhotic  liver,  fatty  or  amyloid  in- 
filtration, the  enlargement  of  muscles  in  pseudohypertrophic 
paralysis,  etc. 

The  term  "hyperplasia"  is  loosely  used  as  has  been  indicated, 
but  is  most  commonly  applied  to  increased  production  of  con- 
nective tissue  in  a  part  or  organ. 

Giant  growth  when  general  is  not  hypertrophy  in  a  true  sense, 
but  rather  an  abnormality  of  development.  Hypertrophy  is  a 
pathologic  change  occurring  in  a  previously  normal  tissue. 

Etiology. — 

1.  Repeated  or  intermittent  pressure. 

2.  Increased  functional  demand.  It  is  called  "work  hyper- 
trophy" when  due  to  increased  exercise,  and  "compensatory 
hypertrophy"  when  an  organ  is  called  upon  to  do  more  work 
because  of  degeneration  or  destruction  of  a  companion  organ 
(as  in  kidney)  or  of  other  parts  (as  heart  when  vessels  are  dis- 
eased), etc. 

3.  Nervous  influence,  as  in  hemihypertrophy  (when  one-half 
of  face  or  body  is  hypertrophied). 

Ill 


112  GENERAL   PATHOLOGY 

4.  Excessive  eating  and  drinking'.  The  heart  is  said  to  en- 
large from  this  cause. 

5.  Obscure  causes,  as  disturbance  of  certain  internal  secre- 
tions, e.g.,  acromegaly  is  associated  with  alteration  in  the  pitui- 
tary body. 

In  so-called  physiologic  hypertrophy,  as  of  mammary  glands  in 
pregnancy,  there  is  no  existing  increased  work  which  causes  the  hy- 
pertrophy, but  rather  the  anticipation  of  such  work,  and  un- 
doubtedly depends  upon  nerve  influence. 

Gross  Pathology. — In  true  hypertrophy,  the  part  is  uniformly 
enlarged  and  consistence  usually  increased.  In  hyperplasia, 
the  increase  in  size  and  consistence  is  apt  to  be  irregular. 

Microscopically,  the  cells  are  increased  in  size  or  number  or 
both.  In  hyperplasia,  there  is  usually  decrease  of  parenchyma, 
with  increase  of  other  tissue  elements. 

Pathologic  Physiology. — In  true  hypertrophy  function  is  in- 
creased— as  secretion,  muscular  power,  etc.  In  hyperplasia, 
function  is  usually  decreased. 

Results. — Hypertrophy  always  reaches  a  limit  sooner  or  later, 
at  which  degeneration  and  atrophy  usually  set  in.  In  some  cases, 
as  in  enlarged  thyroid,  serious  general  disturbance  results. 


CHAPTER  V 1 1 

TUMORS 

In  the  broad  sense  of  the  term,  a  tumor  means  any  form  of 
swelling  of  limited  extent  from  a  dislocated  joint,  pregnant  uterus 
or  hematoma  to  tumors  proper  and  cysts.  In  the  more  restricted 
sense,  however,  as  commonly  used  in  pathology,  a  tumor  may 
be  thus  defined:  A  tumor,  or  neoplasm,  is  an  independent  new 
growth,  without  known  cause,  true  function,  typical  structure  or 
definite  limitation  of  growth.  It  is  independent  of  external  stimu- 
lation or  functional  demand  in  its  development,  and  has  an  ade- 
quate vascular  and  nerve  supply  of  its  own.  It  does  not  increase 
function,  as  does  hypertrophy,  and  the  occasional  secretions  are 
apparently  purposeless.  It  grows  so  long  as  the  body  can  supply 
sufficient  nourishment,  and  may  grow  rapidly  even  when  the  body 
is  wasting. 

Tumors  grow  by  numerical  hypertrophy  of  cells  normal  to  the 
body  at  some  time  or  other  in  its  development;  no  foreign  ele- 
ments are  introduced,  i.e.,  tumors  are  not  "heteroplasms." 

The  structure  of  tumors  is  atypical,  for  while  they  retain 
certain  characteristics  of  the  parent  tissues  from  which  they 
spring,  the  arrangement  and  proportion  of  cells  and  stroma  are 
atypical. 

Theories  of  Origin  and  Causation 

The  Irritation  Theory  (Virchow). — This  accounts  for  about  20 
per  cent  of  tumors,  as  smokers'  cancer  of  the  lips,  scrotal  cancer 
of  chimney-sweeps,  sarcoma  of  injured  bone,  papillomata  of  anal 
and  genital  regions,  etc. 

On  the  contrary,  parts  especially  subject  to  repeated  injuries, 
as  the  hands,  feet,  nipples,  are  rarely  affected. 

The  Inclusion  or  Embryoblastic  Theory  (Cohnheim). — During 
fetal  development,  embryonic  cells  are  included  in  tissues  where 
they  remain  quiescent  as  cell  "rests"  or  "remnants,"  until  some 
irritation  starts  proliferation.  This  theory  explains  dermoid 
cysts,  certain  carcinomata  at  points  of  epithelial  transition,  as  of 

113 


114  GENERAL   PATHOLOGY 

lips,  cervix  uteri,  ehondroid  tumors  in  bone  and  sarcomata  from 
pigmented  moles,  etc. 

However,  many  locations  of  complex  developmental  processes, 
as  in  the  heart  and  nervous  system,  are  seldom  the  seats  of  tumor 
growth. 

The  Parasitic  Theory  (Paget). — This  was  suggested  by  the  fact 
that  many  tumors  give  rise  to  metastasis,  recur  when  removed 
or  may  be  transplanted ;  also  by  reports  that  cancers  have  oc- 
curred in  epidemics,  or  are  contagious  and  hereditary,  but  chiefly 
by  the  fact  that  protozoon-like  bodies  resembling  coccidia,  par- 
ticularly in  Paget 's  disease  of  the  nipple,  have  been  found  in 
certain  tumor  cells.  Many  of  these  bodies,  however,  are  probably 
products  of  cell  activity  or  cell  degeneration,  while  transplanta- 
tion resembles  skin  grafting  too  closely  to  justify  credence  that 
parasites  are  a  factor  in  tumor  transplantation. 

The  Habit  of  Growth  Theory  (Adami)  .—Cells  have  two  func- 
tions— the  performance  of  work  and  reproduction.  During  cell 
reproduction  no  work  is  performed,  and  vice  versa.  Irritation 
Avhether  parasitic  or  otherwise  may  so  modify  the  cell  activities 
that  reproduction  becomes  excessive  and  function  diminishes  or 
disappears. 

The  Nervous  Theory. — Thyroid  tumors  (goiters)  seem  to  de- 
pend upon  nervous  excitement.  Papillomata,  as  warts,  are  known 
to  disappear  by  mental  suggestion.  "Omophobia"  is  a  fear  of 
tumors. 

The  theories  of  Ribbert  (disturbance  of  tissue  tension),  of 
Thiersch  (of  tissue  equilibrium),  of  Billroth  (diathetic — an  ir- 
ritant in  the  circulation — which  has  never  been  demonstrated) 
and  many  others  seem  to  be  purely  speculative. 

Predisposing  Causes.— Age :  Tumors  occur  more  frequently 
after  middle  age.  Of  tumors  occurring  in  early  life  the  connec- 
tive tissue  type  is  the  most  frequent;  in  early  life  the  most  fre- 
quent seats  are  the  eye,  kidney,  bones  and  testicles.  In  adults 
and  the  aged,  the  stomach,  uterus,  liver  and  mammae  are  most 
frequently  affected. 

Sex:  Tumors  in  general  occur  twice  as  often  in  females  as  in 
males,  although  in  regard  to  location,  tumors  of  the  stomach, 
tongue  and  lips  are  more  frequent  in  males. 


TUMORS  115 

Beredity,  occupation,  race  and  climate  are  often  said  to  be  pre- 
disposing causes,  bu1  this  has  never  been  determined. 

The  shape  of  tumors  depends  upon  (a)  the  pressure  of  sur- 
rounding structures;  (b)  its  consistence — the  softer  the  tumor 
the  more  irregular;  and  (c)  the  part  from  which  it  grows;  when 
growing  upon  a  surface,  it  will  form  a  tuberous  growth  (round 
top  with  broad  base),  polypoid  (pendent  with  narrow  pedicle), 
papillomatous  (elongated  with  long  narrow  neck),  (fungous) 
.large  head  and  short  thick  neck),  cauliflower  (irregular  projec- 
tions), dendritic  (a  highly  branched  cauliflower  type),  etc.,  and 
(d)  the  manner  of  growth — centrally  or  peripherally.  "When 
growing  by  proliferation  at  the  center  of  the  tumor,  a  uniform, 
round  swelling  or  node  forms,  which  often  becomes  encapsulated, 
the  surrounding  tissues  being  pressed  aside.  In  peripheral 
growths,  the  surrounding  tissues  are  infiltrated,  the  shape  be- 
comes irregular,  capsules  are  infrequent  and  metastasis  frequent. 

Tumor  growth  is  always  accompanied  by  formation  of  new 
blood  vessels  which  are  usually  thin  and  imperfectly  formed. 

Metastasis  takes  place  when  tumors  are  highly  vascular  and 
cellular,  and  in  those  which  are  not  encapsulated;  it  occurs  via 
the  blood  vessels  when  these  are  in  intimate  contact  with  the 
tumor  cells,  as  in  sarcoma,  or  via  lymphatic  channels  when  these 
are  in  intimate  contact  with  the  cells  as  in  carcinoma.  Metastasis 
is  also  said  to  occur  by  direct  extension  over  certain  surfaces,  as 
serous  surfaces.  Metastatic  tumors  are  malignant,  and  malig- 
nancy means,  in  pathologic  language,  (a)  invasion  of  tissues  by 
infiltration,  (b)  ability  to  cause  metastasis,  (c)  tendency  to  recur 
when  removed,  and  (d)  the  injurious  effects,  other  than  mere  pres- 
sure suffered  by  the  patient,  such  as  general  anemia,  or  some 
form  of  intoxication.  Such  a  condition  is  called  cachexia.  Sar- 
comata and  carcinomata  are  the  types  of  malignant  tumors. 

Benign  tumors  are  such  as  do  not  invade  tissues,  do  not  me- 
tastasize or  recur  when  removed,  but  usually  become  encap- 
sulated and  do  harm  only  by  their  pressure  upon  other  tissues 
or  organs,  or  by  gradually  sapping  the  strength  of  the  patient. 

A  primary  tumor  is  one  originating  at  the  site  in  which  it  is 
found.  A  secondary  tumor  is  one  originating  by  metastasis  of 
cells  (cell  emboli)  from  a  primary  tumor.     Primary  tumors  may 


11 G  GENERAL   PATHOLOGY 

be  multiple,  but  usually  are  single;  secondary  tumors  are  almost 
invariably  multiple. 

Degenerative  changes  occur  in  tumors  as  they  do  in  the  tis- 
sues from  which  they  spring. 

Classification  of  Tumors. — Many  different  classifications  have 
been  suggested.  In  Virchow's  Histogenetic  classification,  his 
law  that  "every  tumor  grows  from  previously  existing  cells  of 
the  same  type"  is  made  the  basis  of  classification:  (1)  Histioid 
tumors — those  growing  from  one  kind  of  tissue  only,  as  fibroma. 
(2)  Organoid  tumors — those  growing  from  parenchymatous  and 
connective  tissues,  as  cancer.  (3)  Teratoid  tumors  (or  syste- 
moid) — those  made  up  of  combinations  simulating  a  system,  as 
dermoid  cysts. 

Cohnheim's  embryoblastic  classification  divides  tumors  accord- 
ing to  their  epiblastic,  hypoblastic  or  mesoblastic  origin,  but  no 
note  is  here  taken  of  the  fact  that  many  tumors  similar  in 
histology  and  function  are  derived  from  all  the  layers  of  the 
blastoderm,  and  vice  versa. 

Adami's  modification  endeavors  to  remedy  this  defect,  and  is 
considered  by  Beattie  and  Dickson  as  the  "most  complete  and 
scientific  classification  compatible  with  present  knowledge." 
First  the  tissues,  embryologically  considered  are  divided  into  (a) 
lepidic  ("rind")  or  lining  membrane  group,  without  lymph  or 
blood  vessels  or  stroma  between  the  cells;  and  (b)  hylic  ("pulp") 
or  body  framework  group.  The  tumors  are  divided  in  lepidomata, 
including  the  papillomata,  adenomata,  carcinomata  and  endothe- 
liomata,  and  hylomata,  including  neuromata,  gliomata,  sarcomata, 
myomata,  fibromata  and  other  connective-tissue  tumors. 

The  commonest  and  perhaps  the  most  practical  classification  is 
that  which  is  based  upon  the  type  of  tissue  involved : 

1.  Connective  tissue ;  fibroma,  myxoma,  chondroma,  osteoma, 
lipoma.    Embryonic  or  malignant  type — sarcoma. 

2.  Muscle  tissue;  leiomyoma  and  rhabdomyoma. 

3.  Nerve  tissue;  glioma  and  neuroma. 

4.  Vascular  tissue ;  angioma — hemangioma  and  lymphangioma. 

5.  Epithelial  tissue;  papilloma  and  adenoma.  Embryonic  or 
malignant  type — carcinoma. 

6.  Teratomata  or  complex  new  growths. 


TUMORS  117 

Fibromata 
Fibromata  are  tumors  composed  of  wavy  bundles  of  connec 

I  ive  tissue. 

Etiology.  Some  of  these  tumors  result  from  injury  or  contin- 
ued irritation;  the  causation  of  others  is  obscure. 

The  favorite  seats  are  the  subcutaneous  and  submucous  tis- 
sues, periosteum,  sheaths  of  tendons  and  nerves,  uterus,  ovaries, 
kidney,  heart,  dura  mater,  etc. 

There  are  two  types  of  these  tumors — the  hard  and  the  soft. 

Gross  Pathology.— Hard  fibromata  vary  in  size  from  a ■  minute 
point  to  a  fist;  they  are  sometimes  lobulated  and  frequently  mul- 
tiple; are  pale,  firm,  cutting  like  leather.      On  section,  surfaces 


Fig.   31. — Hard  fibroma.      (Warren.) 

show  irregular  bands  or  whorls  of  fibers,  often  resembling  the 
grain  in  wood.     They  are  usually  encapsulated. 

A  subvariety  is  the  "painful  subcutaneous  tubercle,"  being 
about  the  size  of  a  coffee  bean,  very  firm  and  circumscribed. 

Fibromata  of  the^  uterus  are  a  combination  of  fibroma  and 
myoma,  often  called  fibromyoma,  or  simply  "fibroid."  These 
may  become  very  large,  weighing  fifty  pounds  or  more;  are  usu- 
ally multiple  and  very  hard. 

Keloids  are  hard  subcutaneous  fibromata,  of  irregular  star- 
like outline,  not  encapsulated,  but  tend  to  spread:  they  often  look 
like  the  scars  of  burns,  and  usually  arise  from  scars  in  those 
who  manifest  a  congenital  predisposition.  Keloids  occur  oftenest 
in  negroes. 


118  GENERAL   PATHOLOGY 

Microscopically  are  seen  dense,  matted,  fibrous  bands  with  rel- 
atively few  cells;  blood  vessels  are  few  and  have  thick  fibrous 
walls,  but  no  muscular  or  elastic  coat.  When  cut  transversely 
the  bundles  have  a  granular  appearance.    (Fig.  31.) 

The  soft  fibromata  are  usually  found  in  subcutaneous  tissues 
and  the  submucous  tissue  of  the  pharynx  and  digestive 
tract.  In  gross  appearance  they  are  usually  larger  than  hard 
fibromata,  soft  and  pink  on  section.  Frequently  they  are  poly- 
poid in  form.  Microscopically  a  loose  fibrillar  network  is  seen, 
with  stellate  and  spindle  cells  irregularly  distributed  and  some- 
times in  islands.    The  vessels  have  distinct  walls.    (Fig.  32.) 


Fig.   32. — Soft  fibroma  of  the  subcutaneous  tissue.      (Stengel  and  Fox.) 

Molluscum  fibrosum  (neurofibromatosis)  is  a  soft  fibromatoid 
growth  occurring  along  the  course  of  subcutaneous  and  submucous 
nerves.  They  range  in  size  from  a  pinhead  to  an  orange  and 
are  usually  multiple. 

Degenerations. — These  are  the  same  as  those  which  occur  in 
normal  fibrous  tissues — hyaline,  mucoid,  fatty,  calcareous  and 
liquefaction. 

Results. — A  fibroma  is  usually  very  slow  in  growth  and  benign. 
If  very  large  it  may  cause  pain  or  pressure  symptoms,  or  even 
death  from  hemorrhage,  exhaustion  or  absorption  of  degeneration 
products.  Fibromata  do  not  recur  when  removed,  except  keloids 
and  certain  polypoid  new  growths,  though  keloids  may  disappear 
spontaneously  or  upon  continued  pressure. 


TUMORS  119 

Myxomata 

Myxomata  are  tumors  composed  of  mucoid  tissue  Mucoid  tis- 
sue is  the  precursor  of  connective  tissue  in  fetal  life. 

Etiology. — Chronic  irritation  may  cause  some  forms,  but  the 
etiology  is  obscure.  Myxomata  usually  occur  in  adult  life.  bu1 
may  be  congenital. 

The  favorite  seats  are  the  subcutaneous  tissues,  especially  of 
the  mammary  gland;  also  submucous  tissue,  especially  nasal;  in- 
termuscular septa,  nerve  sheaths,  brain  and  spinal  cord. 

In  gross  appearance  these  tumors  are  pale  gray  or  reddish 
white  tuberous  or  polypoid  growths,  soft  and  gelatinous  on 
section,  exuding  a  mucous   material  on  pressure.     The   growth 


Fig.  33. — Section  of  a  myxosarcoma,     a,  myxomatous  tissue;  b,  strands  of  cells;  c,  fibrous 

tissue.      (Ziegler.) 

is  usually  well  circumscribed  and  encapsulated,  varying  in  size 
from  a  cherry  to  a  walnut,  though  sometimes  larger.  Occasionally 
the  growth  is  diffuse  and  noncapsulated. 

Microscopically,  irregular  stellate  cells  with  long  anastomosing 
processes  are  seen  lying  within  a  transparent  or  slightly  granular 
material;  the  vascular  supply  is  usually  poor,  though  the  vessels 
are  large  and  thin  walled.     (Fig.  33.) 

Results. — The  growth  is  slow  and  benign,  but  is  often  associated 
with  sarcoma  (myxosarcoma)   or  with  cancer  (carcinoma  niyxo- 


120  GENERAL   PATHOLOGY 

matodes)    which  is  malignant.     Hemorrhage   may   convert   this 
form  of  tumor  into  a  blood  cyst. 

Chondromata 

Chondromata  are  tumors  composed  of  cartilage. 

Etiology. — Irritation  and  trauma  account  for  some  cases.  In 
others  remnants  of  cartilaginous  tissue  deposited  in  abnormal 
places,  as  in  the  parotid  gland,  or  left  unconverted  in  the  de- 
velopment of  bone  form  the  starting  point  for  these  tumors,  while 
congenital  predisposition  and  heredity  also  play  a  part.  They  are 
often  associated  with  rickets,  and  are  rare  after  puberty. 

Two  chief  types:     (l)Ecchondromata  (ecchondroses)   are  out- 


Fig.   34. — Chondroma  of  the  thumb.      (Warren.) 

growths  from  the  perichondrium,  occurring  oftenest  at  the  epi- 
physeal attachments  of  long  bones,  especially  the  phalanges  of 
the  hands,  also  at  the  interpubic  and  occipitosphenoidal  junctions. 
They  occur  also  as  outgrowths  from  articular  cartilages  or  syno- 
vial membranes  in  rheumatoid  arthritis.  (2)  Chondromata,  or 
enchondromata,  originate  in  noncartilaginous  tissues,  usually 
boiie,  but  also  glandular  organs  as  the  parotid  gland,  testicle, 
ovary,  and  in  muscles  and  tendons  near  their  bony  attachments. 
Gross  Morbid  Anatomy. — Chondromata  are  hard,  resistant  to 
the  section  knife,  and  vary  in  size  from  small  nodes  to  large 
tumors.  The  ecchondromata  are  apt  to.be  very  irregular  out- 
growths, often  multiple,  and  firmly  or  loosely  attached  to  the 
tissues  from  which  they  spring,  and  occasionally  even  detached. 


TUMORS  ]21 

TiH.  enchondromata  are  rounded  growths,  often  lobulated  when 
large,  the  Lobules  separated  by  connective  tissue  which  carries  the 
blood  vessels.    (Fig.  34.) 

Microscopically,  the  tissue  resembles  hyaline  cartilage,  Less 
often  white  fibrous  or  elastic  cartilage.  The  cells  are  Less  regu- 
larly arranged  than  in  aormal  cartilage.  Association  with 
myxoma  or  sarcoma  is  frequent.  Calcification  or  ossification  also 
frequently  occur. 

Results.— These  tumors  are  usually  benign  except  when  com- 
bined with  sarcoma,  but  occasionally  metastasis  occurs  even  in 
pure  chondromata,  the  secondary  growths  being  found  usually 
in  the  lungs.    Degeneration  with  cyst  formation  is  frequent. 

Chordomata 

Chordomata  are  tumors  arising  from  the  remains  of  the  noto- 
chord  or  chorda  dorsalis.  They  are  found  principally  about  the 
intervertebral  disks  and  base  of  skull,  and  are  seldom  more  than 
one-half  inch  in  diameter.  These  tumors  resemble  cartilage  gen- 
erally, but  with  ''balloon-like"  cells  having  small  distinct  nuclei, 
and  apt  to  be  vacuolated. 

Osteomata 

Osteomata  are  tumors  composed  of  osseous  tissue. 

Etiology. — Osteomata  occur  at  any  time  of  life ;  irritation  and 
trauma  account  for  some  cases,  and  heredity  seems  to  play  a  part, 
especially  in  the  multiple  osteomata  of  early  life. 

There  are  two  chief  types:  (1)  Hyperostoses,  which  are  in- 
flammatory outgrowths,  including  exostoses  (wart-like  out- 
growths) and  osteophytes  (flat,  extensive  and  loosely  attached 
outgrowths).  These  outgrowths  spring  from  preexisting  bone 
and  are  usually  traumatic  in  origin.  (2)  Osteomata  proper,  which 
may  spring  from  hone  (homoplastic)  or  from  nonosseous  tissue 
(heteroplastic),  such  as  the  testicle,  ovary,  and  meninges. 

Gross  Pathology. — As  in  chondromata,  a  sharp  distinction  can 
not  always  be  drawn  between  the  inflammatory  outgrowths  and 
the  true  tumors,  although  the  tumors  are  usually  more  rounded, 
more  tumor-like  in  outline,  and  when  large  are  apt  to  be  lobu- 
lated. According  to  their  density  osteomata  are  (a)  hard  or 
compact,  resembling  the  outer  layer  of  long  bones,  and  (b)  soft, 


122  GENERAL   PATHOLOGY 

cancellous  or  spongy,  resembling-  the  inner  cancellous  bony  tis- 
sue with  a  shell  of  compact  bone  on  the  exterior.     (Fig.  35.) 

A  sub  variety — eburnated  (ivory-like)  osteomata — consists  of 
very  hard  and  usually  multiple  growths,  occurring  on  the  inner 
table  of  the  skull  bones  (here  often  syphilitic  in  origin),  in  the 
antrum  of  Highmore  and  elsewhere. 

Microscopically,  these  tumors  resemble  bony  tissue,  but  the 
Haversian  canals  and  blood  vessels  are  usually  quite  irregular  and 
smaller  than  in  normal  bone. 

Associations  with  chondromata,  myxomata,  fibromata,  and  sar- 
comata are  frequent,  and  degenerative  changes,  as  softening  and 
necrosis,  occur. 


Fig.   35. — Osteoma   of  the   lower  jaw.      (Warren.) 

Odontomata 

Odontomata  are  tumors  growing  from  the  pulp  of  teeth,  and 
are  not  strictly  osteomata. 

Lipomata 

Lipomata  are  tumors  composed  of  fatty  tissue. 

Etiology — The  etiology  is  not  known.  Usually  they  appear  in 
adult  or  middle  life,  but  sometimes  in  childhood  and  occasionally 
congenitally. 

Lipomatosis  is  a  condition  in  which  there  is  local  diffuse  fatty 
growth  in  certain  parts.  Obesity  is  the  general  increase  of  fatty 
deposits  throughout  the  body. 


TUMORS  12'j 

The  usual  seats  are  the  subcutaneous  tissues  of  the  back,  shoul- 
ders, buttocks  and  limbs,  also  submucous  and  subserous  tissues 
and  the  mammary  glands. 

Gross  Pathology. — A  lipoma  is  a  circumscribed,  encapsulated 
tumor,  usually  lobulated  with  connective-tissue  septa.  On  the 
exterior,  the  new  growths  are  somewhat  hemispherical,  rarely 
polypoid,  and  movable.  They  vary  in  size,  and  may  beeome 
(mormons.  In  the  interior  of  the  body  they  are  usually  polypoid, 
and  oeeasionally  found  detaehed. 

Microscopically,  lipomata  resemble  fatty  tissues  in  general,  al- 
though the  cells  are  larger,  and  large  thin-walled  vessels  are 
seen. 

Results. — These  tumors  are  benign,  although  recurrence  may 
take  place  after  removal.  Calcification  and  less  often  softening 
occur.  The  fat  of  lipomata  is  not  used  by  the  system  in  starva- 
tion. 

Sarcomata 

Sarcomata  are  tumors  composed  of  connective  tissue  of  the  em- 
bryonic type,  having  very  little  intercellular  substance  and  a 
large  number  of  cells. 

Etiology. — These  tumors  occur  in  youth  and  early  adult  life, 
and  are  sometimes  congenital.  Some  cases  follow  traumatism. 
They  are  more  frequent  in  males. 

Locations. — Sarcomata  are  found  in  the  subcutaneous,  perios- 
teal, tendinous,  and  muscular  tissues;  in  bone,  cartilage,  lymph 
glands,  submucous  and  subserous  tissue;  in  the  kidneys,  liver, 
spleen,  thyroid,  testes,  etc. 

Gross  Pathology. — Sarcomata  are  more  or  less  rounded,  usually 
without  demarcation  between  them  and  the  surrounding  tissues, 
although  when  fully  developed,  or  when  growth  is  slow,  a  cap- 
sule or  apparent  capsule  may  form.  Superficial  tumors  are  apt 
to  be  flat  or  irregular  elevations;  typically  a  sarcoma  is  flesh- 
like  in  appearance  when  sectioned,  pink  in  color,  though  many 
are  pale  or  gray.  Dilatation  of  blood  vessels  may  cause  a  hemor- 
rhagic appearance,  and  actual  hemorrhages  into  the  tumor  are 
frequent.  Sarcomata  infiltrate  adjacent  tissue  and  are  not  readily 
movable.  They  may  be  hard  or  soft  according  to  the  relative 
amounts  of  cells  and  intercellular  substance.  A  whitish  liquid 
exudes  on  section. 


124  GENERAL   PATHOLOGY 

Pathologic  Histology. — The  cells  are  round,  cylindrical,  spin- 
dle-shaped, or  polymorphous,  and  contain  large  vesicular  or  gran- 
ular nuclei.  Mitotic  figures  may  he  seen  in  rapidly  growing 
tumors — less  commonly  amitotic  division  occurs.  Nuclear  de- 
generation is  frequent.  The  cells  are  irregularly  arranged,  though 
occasionally  in  more  or  less  parallel  columns.  The  intercellular 
substance  is  scant,  homogeneous  with  few  or  no  distinct  fibers, 
and  found  in  immediate  relation  with  the  cells,  thus  differing 
from  carcinoma. 

The  blood  vessels  usually  consist  of  a  single  endothelial  coat, 
though  in  some  cases  they  are  more  fully  developed  and  form 
the  skeleton  of  the  tumor ;  they  penetrate  the  tumor  tissue  and 
come  in  direct  contact  with  the  cells  (again  differing  from  car- 
cinoma)— in  fact,  parts  of  the  tumor  may  grow  into  the  vessels 
permitting  the  blood  to  circulate  in  clefts  ;nnong  the  tumor  cells; 
hence  sarcomata  metastasize  through  the  blood  vessels  as  a  rule, 
while  carcinomata  which  have  more  distinctly  formed  blood  ves- 
sels metastasize  through  the  lymphatics. 

Association  with  other  tumors,  especially  of  the  connective 
type  is  frequent. 

Results. — Sarcomata  are  malignant  as  a  rule.  The  round-celled 
and  melanotic  are  the  most  malignant — the  giant-cell  and  fibro- 
sarcomata  are  the  least  malignant.  In  general  the  smaller  the 
tumor  cells,  the  more  malignant  the  tumor.  Degenerations, .as 
myxomatous,  liquefaction,  blood  cysts,  etc.,  occur  frequently. 
Anemia,  leucocytosis  and  fever  often  attend  the  disease. 

Sarcomata  are  classified  as  follows: 

1.  Round-celled  sarcomata — both  large-celled  and  small-celled, 
including  lymphosarcomata.  most  of  the  alveolar  sarcomata,  an- 
giosarcomata  and  sarcomatous  cylindromata. 

2.  Spindle-celled  sarcomata — large-celled  and  small-celled,  in- 
cluding a  few  alveolar  sarcomata. 

3.  Melanotic  sarcomata. 

4.  Giant-celled  sarcomata. 

Round-celled  Sarcomata 

Round-celled  sarcomata  are  usually  found  in  loose  connective 
tissues  in  viscera,  as  kidney,  ovary,  brain,  lymphatic  nodes,  otc. 


TUMORS 


125 


Grossly  they  are  white,  gray  or  pink,  soft,  usually  rounded 
and  well-defined  but  not  encapsulated;  they  bleed  easily,  are 
often  quite  soft  and  cheesy  in  the  center,  the  small-celled  being 
softer  than  the  large-celled  tumors. 

Histologically,  the  cells  when  small  resemble  lymphoid  cells. 
There  is  no  fundamental  difference  between  the  small-celled  and 
large-celled  varieties;  in  the  latter  the  cells  are  larger  with  rel- 
atively more  cytoplasm,  the  nuclei  stain  less  deeply,  the  inter- 
cellular substance  is  more  fibrillar,  and  the  blood  vessels  are  fewer 
but  better  supported  than  in  the  small-celled  variety. 

The  lymphosarcoma  is  a  small  round-celled  sarcoma  occurring 
in  lymph  nodes,  lymph  adenoid  tissue,  and  sometimes  in  other 
organs,  as  the  thyroid,  thymus  and  salivary  glands.  It  resembles 
a  lymph  node  in  appearance  and  structure,  the  chief  distinguish- 


Fig.    36. — Small    round-celled   sarcoma:    in   the   center  is   seen   a  blood   vessel   with   its   wall 
of    endothelium.      (Stengel    and    Fox.) 

ing  feature  being  its  tendency  to  spread  beyond  the  capsule  or 
normal  limitations  of  the  nodes  or  organs,  and  in  case  of  the 
lymph  nodes,  causing  the  separate  nodes  to  fuse  together,  ob- 
literating the  normal  appearances,  as  germ  centers,  cortex,  and 
medulla. 

The  alveolar  sarcoma  is  grossly  similar  to  other  forms  of  sar- 
coma and  occurs  mainly  in  lymph  nodes  and  serous  membranes, 
moles  of  the  skin,  warts,  etc.  Histologically  there  are  trabecu- 
le of  spindle-shaped  cells  and  intercellular  substance,  dividing 
the  tumor  into  alveoli  containing  round  sarcoma  cells.  Blood 
vessels  traverse  the  trabecule  and  rarely  if  ever  enter  the  cell 
groups.  These  tumors  are  difficult  to  differentiate  from  car- 
cinomata,  though  in  the  latter  the  blood  vessels  are  said  to  be 
usually  better  developed. 


126 


GENERAL   PATHOLOGY 


Angiosarcomata  spring  from  the  adventitia  of  blood  vessels. 
They  occur  in  1  lie  salivary  glands,  serous  membranes,  and  in  the 
skin,  and  consist  of  round-celled  masses  surrounding  the  blood 
vessels.  These  tumors  are  more  or  less  benign,  but  often  become 
melanotic  and  malignant. 

"Cylindroma"  originally  meant  any  tumor  "showing  gelat- 
inous  masses  or   trabecule   traversing;  its   substance,"   but   dif- 


\ 


I'ig.    37. — Large   rout 


(  DrlalirM    and    I'iik 


ten.) 


Fig.    38. — Alveolar   sarcoma.      (Warren.) 


ferent  histologic  structures  are  described  under  this  name.  Sar- 
comatous cylindromata  may  be  defined  as  sarcomata  in  which 
hyaline  and  myxomatous  degeneration  have  occurred  in  more  or 
less  insular  collections;  also  as  angiosarcomata  with  similar  de- 
generation of  the  sarcomatous  cells  surrounding  the  vessels,  re- 
sulting in  either  case,  in  branching  cylinders  of  gelatinous  ma- 
terial throughout  the  tumor.     (Figs.  36,  37,  and  38.) 


TUMORS 


127 


Spindle-celled  Sarcomata 

Spindle-celled  sarcomata  occur  in  dense  tissues,  as  periosteum, 
tendons,  fasciae,  less  often  in  loose  I  issues.  Grossly,  they  are 
harder  than  the  round-celled  tumors,  and  more  grayish  and  flesh- 
tinted.  The  cells  are  spindle-shaped  with  tapering  ends  and 
sometimes  branching  extremities,  and  apt  to  be  arranged  in  par- 
allel rows.  In  the  small-celled  variety,  the  intercellular  sub- 
stance is  less  fibrillar  and  the  blood  vessels  more  imperfect  than 
in  the  large-celled  form.    (Fig.  39.) 

When  the  intercellular  fibrils  become  very  evident,  it  is  called 


Fig.   39. — Spindle-cell   sarcoma   of   the   mammary  gland.      Oc.    3;    ob.   9.      (McFarland). 


fibrosarcoma.     The  so-called  "recurring  fibroids"  are  fibrosar- 
comata. 

Melanotic  Sarcoma,  or  Melanomata 

Melanotic  sarcomata,  or  melanomata,  spring  from  some  pig- 
mented tract,  as  the  uveal  tract  of  the  eye,  pigmented  mole,  etc. 
The  cells  contain  metabolic  pigment  (melanin)  varying  greatly 
in  amount,  and  distributed  uniformly  or  in  patches.  The  nuclei 
are  poor  in  chromatin  and  show  a  distinct  network.  These  tu- 
mors are  very  malignant,  metastasize  to  any  tissue,  but  chiefly 


128 


GENERAL   PATHOLOGY 


through  the  lymphatics  to  the  lymph  nodes.    Sometimes  the  cells 
are  epithelioid  and  arranged  in  alveoli. 

Giant-celled  Sarcomata 

Giant-celled  sarcomata  are  composed  of  spindle  or  round  cells 
with  a  variable  number  of  giant  cells.  They  spring  from  the 
medulla  of  long  bones,  are  circumscribed,  and  usually  encap- 
sulated; may  be  firm  or  soft,  reddish-brown  on  section  and  some- 
what fibrous.  They  occur  oftenest  in  the  young,  at  the  lower 
end  of  the  femur,  upper  tibia,  lower  radius  and  lower  jaw  (one 
form  of  epulis).     (Figs.  40,  41,  42  and  43.) 

Two  rare  forms  of  connective  tissue  tumors  are: 


Fig.    40. — Large    spindle-celled   sarcoma.      (Delafield   and    Prudden.) 

1.  Xanthoma,  which  is  a  lipoma  with  large  fat  cells  and  a 
certain  amount  of  round-celled  infiltration,  and  of  a  peculiar 
yellowish  color;  is  found  usually  about  the  eyelids,  and  occa- 
sionally in  diabetes,  more  generally  distributed. 

2.  Chloroma,  which  is  a  variety  of  lymphosarcoma  or  round- 
celled  sarcoma,  occurring  in  the  periosteum  of  the  bones  of  the 
head,  especially  the  orbit,  and  having  a  peculiar  greenish  color; 
it  is  malignant,  giving  rise  to  secondary  tumors  in  lymphadenoid 
tissue  and  especially  the  bone  marrow. 


TUMORS 


12«J 


V 


Fig.   41.— Melanosa 


Stengel    and    Fox.) 


Fig.  42. — Giant  cell  sarcoma  of  the  thigh,     a,   giant  cells;    b,  spindle   cells.      (McFarland.) 


130  GENERAL   PATHOLOGY 

Rhabdomyomata 

Bhabdomyomata  are  tumors  containing  striped  muscle  tissue. 
They  are  rare  and  usually  congenital.  In  the  genitourinary  sys- 
tem, they  are  probably  due  to  the  inclusion  of  lumbar  muscle 
fibers.  Their  favorite  seats  are  the  kidneys,  testicle  and  other 
parts  of  the  genitourinary  tract,  also  heart  muscle,  lumbar  and 
gluteal  muscles.  The  tumors  are  round  or  irregular  in  shape 
and  more  or  less  encapsulated,  and  if  superficial,  pedunculated. 
Microscopically  the  muscle  fibers  are  imperfectly  developed  and 


Fig.    43. — Metastatic   melanosarcoma   of   lung,    showing  pigmented   and    nonpigmented    nod- 
ules  (from  a  specimen  in  the  possession  of  Dr.  Allen  J.   Smith.) 

associated  with  a  varying  amount  of  connective  tissue.  When 
the  latter  becomes  embryonal  in  type,  a  rhabdosarcoma  develops, 
which  is  much  more  frequent  than  the  pure  rhabdomyoma. 

Leiomyomata 

Leiomyomata  are  tumors  containing  smooth  muscle  fibers. 
They  spring  from  preexisting  smooth  muscle,  usually  of  an  organ 
or  the  media  of  blood  vessels.  In  the  uterus  it  may  arise  from 
congenital ly  misplaced  portions  of  the  Wolffian  body  or  ducts  of 
Mueller. 


TUMORS 


131 


The  favorite  locations  are  the  uterus,  gastrointestinal  tract, 
ovaries,  less  often  blood  vessels,  sk in,  nipples,  etc. 

Gross  Pathology.  -The  I  iimors  are  firm,  rounded,  nodular  masses, 
closely  resembling  fibromata,  but  usually  darker  in  color, 
and  varying  in  size  up  to  many  pounds.  The  large  tumors  are 
usually  a  combination  of  myoma  and  fibroma — a  fibromyoma, 
such  as  the  uterine  "fibroid"  which  may  grow  to  an  enormous 
size      Leiomyomata    are    encapsulated,    and   on   section   have    a 


) 


V 


Fig.  44. — Submucous  fibroid  in  the  uterus.  The  tumor  forms  a  large  mass  in  the  in- 
terior of  the  organ  whose  wall  is  much  attenuated  at  the  fundus.  The  cervix  is  nearly- 
normal  in  size,  though  somewhat  altered  in  shape.  The  ovaries  and  tubes  which  are  still 
attached  are  normal.      (McFarland.,) 

striated  appearance,  the  striae  being  concentrically  arranged  or 
in  a  wave-like  manner.  They  are  usually  grayish  or  flesh-colored, 
but  may  be  red,  due  to  dilated  blood  vessels. 

Uterine  fibromata  are  usually  multiple,  and  either  submucous, 
interstitial  (intramural),  or  subserous  in  origin.  The  intramural 
tumors  do  not,  as  a  rule,  project  from  either  surface  of  the  uterus. 
Uterine  fibromata  occur  oftenest  during  the  third  or  fourth  dec- 


132  GENERAL   PATHOLOGY 

ades  of  life,  and  continue  to  increase  in  size  up  to  the  time  of 
the  menopause,  thereafter  usually  decreasing.     (Fig.  44.) 

Leiomyomata  of  the  skin  occur  in  young  adults,  or  even  in 
children.    They  are  multiple  and  often  painful. 

Histologically,  bundles  of  muscle  cells  are  seen,  running  in  dif- 
ferent directions  and  having  cylindrical  nuclei.  Sometimes  elas- 
tic tissue  elements  are  present,  and  nearly  always  connective 
tissue  cells.  Blood  vessels  are  scant,  though  often  with  well  de- 
veloped middle  coats.  Calcification  is  common,  especially  in 
uterine  fibromata  ("womb  stones")  preceded  by  hyaline  or  fatty 
change. 

Results. — Growth  is  slow  and  the  tumors  are  benign,  although 
sarcomatous  change  may  add  a  malignant  character. 

ilk 

I  **% 

£*■:•«     *- 

Fig.    45. — Glioma    of    the    brain.       (Delafield    and    Prudden.) 

Glioma 

Glioma  is  a  tumor  composed  of  neuroglia. 

The  favorite  seats  are  the  brain  and  cord,  optic  tract,  nerve 
and  retina,  and  parts  of  the  olfactory  tract.  Glioma  of  the  retina 
occurs  usually  between  the  second  and  fourth  year  of  life.  (Fig. 
45.) 

Gross  Pathology. — Gliomata  are  usually  single,  rounded  masses, 
gradually  merging  into  surrounding  tissue.  Somewhat  harder 
than  brain,  their  color  is  but  slightly  changed,  though  some- 
times dark  red.  They  vary  in  size  from  a  pea  to  a  lemon.  Glioma 
of  retina  may  extend  to  eyeball  or  along  optic  nerve. 

Pathologic  Histology. — Great  numbers  of  cells  are  seen  with 
round  or  oval  nuclei  and  with  scant  cytoplasm  (glia  cells).  They 
are  usually  larger  than  the  normal  neuroglia  cells.  Fine  wavy 
fibrils  (neuroglia)   lie  parallel  to  the  axes  of  the  cells  to  which 


TUMORS  133 

they  are  attached  at  the  sides,  the  cuds  of  the  fibrils  being  free. 
In  the  I'd  inn.  the  cells  are  similar  to  its  granular  layer. 

Results.-  Benign,  1ml  may  be  dangerous  from  pressure  or  loca- 
1  ion.    Glioma  of  eye  may  recur  after  removal. 

Glioma  Ganglionare,  or  Ganglionic  Glioma,  or  Neuroma 

This  is  a  mixed  tumor  composed  of  neuroglia,  nerve  fibers,  and 
ganglionic  cells.  It  usually  occurs  in  multiple  nodular  growl  lis 
throughout  the  brain  and  cord,  or  in  the  sympathetic  ganglia, 
varying  in  size  from  that  of  a  millet  seed  to  that  of  an  apple. 

Gliomatosis  is  a  diffuse  proliferation  of  glia  throughout  the 
central  nervous  system. 

Neuroma  occurs  in  two  forms — true  and  false. 

True  neuroma  is  a  very  rare  tumor  composed  of  nerve  fibers. 

False  neuroma  (the  common  form)  is  a  fibrous  tumor  spring- 
ing from  the  perineurium  and  endoneurium  of  nerves. 

The  etiology  is  not  known,  though  traumatism  accounts  for 
amputation  neuromata.  They  are  usually  found  upon  the  periph- 
eral nerves,  but  may  occur  in  any  part.  Sometimes  the  nerves 
are  involved  near  their  roots,  or  at  their  endings  within  organs. 

Gross  Pathology. — False  neuromata  are  usually  found  as  mul- 
tiple thickenings  along  the  course  of  nerves.     They  may  occu 
in  the  form  of  a  network  (plexiform  neuromata).     After  ampu- 
tation small,  rounded  growths  occur  at  the  ends  of  some  of  the 
nerves,  are  firm  and  not  sharply  circumscribed. 

Pathologic  Histology. — False  neuromata  are  composed  of  re- 
ticulated connective  tissue,  pushing  aside  or  surrounding  the 
true  nerve  fibers — the  latter  being  often  degenerated  from  pres- 
sure. True  neuromata  are  composed  of  medullated  fibers  (myelinic 
neuromata)  or  of  nonmedullated  (amyelinic  neuromata).  Ampu- 
tation neuromata  are  usually  a  mixture  of  myelinic  and  false 
neuromata. 

Results. — These  tumors  usually  cause  pain.  They  are  benign, 
though  often  rapid  in  growth. 

Angiomata 

Angiomata  are  tumors  composed  of,  or  following  the  type  of, 
blood  or  lymph  vessels.  Used  alone,  "angioma"  refers  to  the 
hemangioma. 


134 


GENERAL   PATHOLOGY 


Hemangiomata,  or  angiomata,  are  tumor-like  formations  con- 
sisting- principally  of  dilated  and  elongated  blood  vessels,  some 
of  which  may  be  independent  new  growths.  A  certain  amount 
of  connective  tissue  is  always  formed  which  holds  the  vessels  to- 
gether. Usually  the  angioma  is  connected  with  the  general  circu- 
lation through  a  few,  sometimes  but  one,  arterioles  or  veins. 
Three  forms  are  described : 

(a)  Angioma  simplex,  or  Nevus,  which  consists  of  dilated  capil- 


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Fig.  46. — Cavernous  angioma  of  liver.  The  illustration  shows  tumor  tissue  only:  o, 
blood  channels  filled  with  corpuscles;  b,  fibrous  framework  supporting  delicate  walls  of 
blood  sinuses.      (McFarland.) 

laries,  arterioles  and  venules  woven  into  a  plexus.  It  is  usually 
congenital  (birthmarks).  It  may  be  red  in  color  (arterial)  or  dark 
(venous)  ;  pigmented  (pigmented  mole)  or  covered  with  fine  hairs. 
It  may  be  found  on  the  skin,  lips,  tongue,  conjunctivae  and  rarely 
the  meninges. 

(b)  Cavernous  angioma,  or  eavcrnoma,  which  consists  of  widely 
dilated  blood  cavities  separated  by  connective  tissue  partitions  and 
lined  by  epithelium.     It  is  dark  in  color,  larger  than  the  simple 


TUMORS  l?);") 

form,  and  may  pulsate.  II  is  round  most  Frequently  in  the  liver, 
where  it  may  be  multiple,  skin,  breast,  hones  and  internal  organs. 
(Fig.  46.) 

(c)  Plexiform  angioma,  which  consists  of  a  dilatation  and  elon- 
gation of  a  group  of  arteries  of  moderate  size,  and  found  upon  the 
head,  face,  perineum,  legs,  forearm  and  elsewhere.  It  is  in  reality 
a  "congeries  of  cirsoid  aneurysms"  forming  a  tumor-like  enlarge- 
ment. 

Lymphangioma  is  a  tumor-like  formation,  consisting  of  dilated 
lymph  vessels,  rarely  of  newly  formed  lymph  channels.  Three 
forms  are  described: 

(a)  Lymphangioma  simplex,  or  lymphangiectasis,  is  a  simple  dila- 
tation of  a  group  of  lymph  vessels  forming  tumor-like  masses.  A 
congenital  forms  occurs  usually  upon  the  face  and  neck,  and  often 
confined  to  the  papillary  layer  of  the  skin.  The  acquired  form  is 
due  to  lymphatic  obstruction  (as  elephantiasis,  due  to  filarias) 
tending  to  dilatation  of  the  lymph  vessels  and  overgrowth  of  con- 
nective tissue. 

(b)  Cavernous  lymphangioma,  which  corresponds  to  the  caver  - 
noma  of  the  blood  vessels.  It  may  affect  the  tongue  (macroglos- 
sia)  or  lip  (macrocheilia)  or  the  mesentery.  These  conditions  are 
congenital. 

(c)  Cystic  lymphangiectasis,  which  occurs  commonly  about  the 
neck,  as  cystic  hygroma,  consisting  of  multiple  clear  cysts  lined 
with  endothelium  and  having  fibrous  walls. 

Among  special  forms  of  lymphangioma ta  may  be  mentioned 
the  common  pigmented  mole,  which  is  a  slightly  elevated  growth, 
soft  and  flabby,  occurring  on  the  skin  in  early  youth.  It  is  a 
cutaneous  outgrowth  consisting  of  a  stroma  of  fibrous  tissue  and 
containing  pigmented  cells.  When  consisting  of  telangiectatic 
vessels,  it  is  called  a  pigmented  nevus. 

Papillomata 

Papillomata  are  tumors  growing  from  the  papillary  processes, 
Avhich  they  resemble  in  structure. 

Etiology. — Irritation  is  the  cause  of  many,  if  not  all,  of  these 
tumors.  They  are  found  in  the  skin  of  the  back,  neck,  and 
hands,  the  mucous  membranes,  particularly  of  the  bladder,  nose, 
larynx  and  gastrointestinal  tract,  and  glandular   ducts,  as  the 


13G  GENERAL    PATHOLOGY 

female  breasts.  They  also  occur  within  cavities  of  cystic  adeno- 
mata (papuliferous  cysts). 

Gross  Pathology. — Various  forms  are  described:  (1)  Hard 
fibromata,  verruca  or  warts,  occur  singly  or  in  groups  upon  the 
skin.  They  may  be  smooth  or  cauliflower-like  in  outline,  varying 
in  size  from  a  pinhead  to  a  walnut.  (2)  Venereal  warts  or  con- 
dylomata acuminata.  These  occur  about  the  genitals  and  anus, 
rarely  elsewhere,  are  softer,  more  vascular,  and  more  polypoid 
than  the  ordinary  warts,  and  caused  by  gonorrheal  discharges. 
The  condyloma  latum,  or  mucous  patch,  is  also  a  warty  outgrowth 
upon  mucous  membranes  and  moist  dermal  surfaces,  occurring 
during  secondary  syphilis.  (3)  Soft  papillomata  are  usually  seen 
on  mucous  surfaces  as  soft  cauliflower-like  growths,  red,  or  gray 
in  color,  or  sometimes  as  villous  outgrowths.  (4)  Intracystic  papil- 
lomata are  villous  outgrowths  springing  from  the  walls  of  cysts, 
especially  mammary,  thyroid  and  ovarian  cysts.  The  growths 
may  fill  and  greatly  distend  the  cysts  and  occasionally  rupture 
them. 

Pathologic  Histology. — The  normal  relation  of  cells  to  the 
membrana  propria  persists  in  all  papillomata.  There  is  a  cen- 
tral stroma  which  contains  the  vessels  and  is  covered  with 
epithelium — stratified  squamous  in  case  of  skin  growths,  tend- 
ing to  horny  change  and  sometimes  horny  concentric  whorls  or 
pearls.  The  structure  in  the  mucous  membrane  is  the  same 
where  the  epithelium  is  of  the  squamous  type,  as  in  parts  of  the 
larynx,  but  there  is  little  tendency  to  horny  change.  In  the 
gastrointestinal  tract  and  bladder,  the  growths  are  soft  and  vil- 
lous or  dendritic,  and  Ihe  epithelium  is  scant  and  of  the  type 
peculiar  to  the  location.  The  relative  amounts  of  connective  tis- 
sue stroma  and  covering  epithelium  vary;  when  the  latter  pre- 
dominates, it  may  suggest  an  epithelioma,  though  papillomata 
always  tend  to  grow  outward  rather  than  into  deeper  structures. 
Many  of  the  soft  papillomata  are  quite  vascular  and  bleed  easily. 
(Figs.  47  and  48.) 

Results. — Papillomata  are  benign,  but  large  tumors  may  im- 
pair health  by  repeated  hemorrhages,  as  in  the  gastrointestinal 
tract,  or  by  interfering  with  function,  as  in  bladder  or  larynx. 


TUMORS 


137 


Fig.    47. — Papillomata  of  the  vocal   cords    (from   a  specimen   in   the   Museum   of   the   Phila- 
delphia Hospital). 


Fig.   48. 


-Papilloma  of  the  scalp.     The   branching  fibrous  stroma   is   covered   by   an   abnor- 
mally thickened,  irregular  epithelium.     (Boyce.) 


138  GENERAL   TATHOLOGY 

Adenomata 

Adenomata  are  tumors  resembling  in  structure  an  epithelial 
gland  and  developing  from  glandular  epithelium. 

Etiology. — They  are  caused  by  irritation,  as  in  gastrointestinal 
adenomata,  by  tissue  inclusions,  as  in  renal  adenomata.  In 
other  cases  the  causes  are  obscure. 

Their  favorite  seats  are  the  mucous  membrane,  especially  of 
the    pylorus,    duodenum   and    rectum;    the    skin — sebaceous    and 


Fig.  49. — Adenoma  of  the  mamillary  gland,   with  cystic   enlargement  of  acini  and  abundant 
interglandular    hyperplasia    of    connective    tissue.       (Stengel    and    l"ox.) 

sweat  glands;  certain  organs,  as  the  mammary  glands  (the  most 
frequent  seat),  liver,  kidney,  adrenals,  thyroid,  ovary  and  uterus. 
Gross  Pathology. — Adenomata  occur  as  more  or  less  diffuse, 
sessile  growths,  sometimes  pedunculated  or  papillomatous  in 
form;  or  within  organs  as  nodular  tumors,  firm,  usually  single 
and  encapsulated,  capable  of  being  shelled  out,  though  at  times 
adherent.  On  section  the  cut  surfaces  usually  bulge  and 
resemble,  more  or  less,  the  parent  gland,  being  grayish  pink 
in  the  mammae,  and  red  in  the  thyroid  gland. 


tumors  139 

Pathologic  Histology.-  Acini  with  single  layers  of  columnar 
epithelium  (sometimes  several  layers)  are  seen  enclosed  by  con- 
nective-tissue  reticula,  which  contain  the  blood  vessels.  The  ex- 
cretory duds  are  absent  or  poorly  developed. 

When  the  tissue  corresponds  closely  to  the  normal  arrange- 
ment, the  tumor  is  a  simph  adenoma;  when  the  stroma  pre- 
dominates, fibroadenoma;  when  acini  greatly  predominate,  acinose, 
racemost  or  alveolar  adenoma;  when  duels  are  conspicuous,  tubu- 
lar, or  canalicular  adi  noma. 

Results. — Pure  adenomata  are  benign,  but  may  sometimes  cause 
metastasis,  especially  the  hepatic  and  thyroid  tumors.  General 
health  may  suffer  from  hemorrhages,  interference  with  vital  func- 
tions, or  from  ulcerations.  Gastric  and  uterine  adenomata  are 
apt  to  become  carcinomatous.     (Fig.  49.) 

Carcinomata 

Carcinomata  are  tumors  embryonal  or  atypical  in  character, 
which  always  arise  from  epithelial  cells. 

Etiology. — Irritation  accounts  for  some  cases.  They  occur  usu- 
ally after  middle  life,  being  rarely  found  in  early  life  or  child- 
hood. They  are  more  frequent  in  women,  and  in  the  Caucasian 
race.  Tumors  springing  out  of  connective  tissues,  as  bone,  can 
only  be  explained  by  the  inclusion  theory. 

The  favorite  seats  are  the  uterus,  skin,  esophagus,  pylorus,  rec- 
tum, mamma?,  ovaries,  less  often  the  liver,  kidney,  thyroid  gland, 
prostate  and  testicle.  Carcinomata,  however,  may  spring  from 
any  epithelial  tissue. 

Secondary  tumors  usually  do  not  affect  the  parts  in  which 
the  primary  growths  are  frequent,  and  occur  usually  in  the  lymph 
glands,  liver,  spleen,  lungs,  serous  membranes,  and  bones. 

General  Structure. — The  cells  are  very  diverse  in  outline — 
round,  oval,  squamous,  fusiform,  cylindrical,  cuboidal  or  cau- 
date, and  have  large,  clear  nuclei.  Compression  develops  poly- 
hedral forms. 

The  stroma  consists  of  fibrous  tissue,  which  forms  irregular 
spaces,  or  alveoli,  which  communicate  with  one  another,  within 
which  lie  the  cancer  cells  in  branching  or  anastomosing  columns, 
due  probably  to  the  fact  that  cancer  cells  proliferate  along  the 
lymph  channels.     The  stroma  may  be  infiltrated  with  leucocytes 


140  GENERAL   PATHOLOGY 

and  plasma  cells  and  even  mast  cells.  In  slowly  growing  tumors  the 
stroma  is  fibrous;  in  rapidly  growing  tumors  it  approaches  the 
embryonal  or  mucoid  type.  The  stroma  contains  the  blood  ves- 
sels, which  have  distinct  walls  and  do  not  penetrate  the  alveoli. 
The  lymphatics  are  continuous  with  the  alveoli,  thus  affording  a 
ready  means  of  metastasis. 

In  general,  skin  cancers  resemble  enlarged  papillae  penetrat- 
ing into  the  tissues,  and  gland-celled  cancers  resemble  acini  of 
glands,  filled  with  many  layers  of  cells,  but  in  all  cases,  there  is 
noted  the  tendency  of  the  cells  to  penetrate  the  basement  or 
limiting  membrane  and  infiltrate  the  tissues. 

Secondary  carcinomata  are  usually  multiple,  more  circum- 
scribed and  less  infiltrating,  and  as  a  rule  softer  than  the  primary 
tumors. 

The  histologic  differentiation  between  carcinoma  and  sarcoma 
can  not  always  be  made  from  the  morphology  of  the  cells,  for 
they  are  polymorphic  in  both  forms  of  tumor,  and  it  finally  rests 
upon : 

(a)  Grouping  of  the  cells — in  alveoli  in  cancer;  irregularly  in 
sarcoma. 

(b)  Intercellular  fibers — none  in  cancer;  always  a  few  in  sar- 
coma. 

(c)  Position  of  blood  vessels — in  trabecula?  in  cancer;  among 
the  individual  cells  in  sarcoma. 

In  alveolar  sarcoma,  however,  these  distinctions  are  not  so 
evident,  but  here  the  intercellular  fibrillar  may  be  seen  to  be  con- 
tinuous with  the  perialveolar  fibrous  tissue,  and  the  blood  ves- 
sels are  thin-walled  and  not  so  well  supported  as  in  cancer. 

Degenerative  Changes. — These  are  frequent,  especially  fatty  de- 
generation. The  cells  may  be  cloudy,  swollen,  dropsical  or  vacuo- 
lated. Nuclear  degeneration  may  occur,  giving  the  appearance 
of  parasites.  True  colloid  degeneration  may  occur  but  is  very 
rare,  the  term  "colloid  cancer"  usually  refers  to  myxomatous 
change  of  the  stroma.  Liquefaction  may  form  cysts.  Calcifica- 
tion occurs,  especially  in  ovarian  cancers. 

Inflammatory  changes  are  common.  On  free  surfaces,  ulcera- 
tion results  from  traumatism,  irritation  or  infection.  Erysipelas, 
tuberculosis  and  syphilis  may  be  associated.  Hemorrhages  are 
frequent  both  into  the  stroma  and  from  the  ulcerating  surfaces — 


TUMORS  141 

the  latter  are  apt  to  be  extensive  in  cancer  of  the  stomach  and 
uterus. 

Malignancy. — Cancers  are  malignant;  the  medullary  gland- 
celled  being  most,  the  squamous-celled  the  least  malignant.  Me- 
tastasis occurs  through  the  lymphatics,  but  occasionally  through 
the  blood  vessels  (veins)  especially  through  the  portal  vein  to 
the  liver  in  cases  of  intestinal  carcinomata.  Hemorrhages,  hem- 
olysis, and  probably  some  form  of  toxemia  cause  the  anemia  and 
cachexia  so  characteristic  of  these  tumors. 

Carcinomata  are  divided  into: 

1.  Epithelioma ta,  or  squamous-celled  carcinomata. 

2.  Gland-celled  carcinomata: 

(a)  Adenocarcinomata,  or  cylindric-celled  carcinomata. 

(b)  Hard,  scirrhous,  fibrous,  or  chronic  carcinomata. 

(c)  Soft,  medullary,  encephaloid  or  acute  carcinomata. 

(d)  Carcinoma  simplex,  or  simple  cancer. 

Epithelioma 

Epithelioma  is  found  in  the  skin  and  squamous  mucous  mem- 
branes, especially  the  lip,  nose,  tongue,  esophagus,  pharynx  and 
cervix  uteri.  It  is  apt  to  develop  where  different  types  of  epi- 
thelium join. 

Gross  Pathology. — Irregular,  hard,  wart-like,  immovable  ele- 
vations are  seen,  which  tend  to  ulcerate,  exuding  a  sanious  fluid. 
On  section  they  are  firm  and  comparatively  bloodless. 

Pathologic  Histology. — Irregular,  branching  columns  of  squa- 
mous cells  are  seen,  though  pressure  may  alter  their  shape,  ex- 
tending from  the  papillae  down  into  the  deeper  tissues.  In  normal 
skin  the  cells  spring  from  the  rete  malpighii,  and  become  flat- 
tened and  horny  as  they  proceed  outward,  but  in  the  tumor 
instead  of  growing  outward  toward  a  free  surface,  they  are 
packed  in  more  or  less  rounded  masses,  the  older  cells  being 
forced  to  the  center  and  becoming  cornifled,  thus  forming  the 
concentric  whorls  or  "epithelial  pearls"  so  characteristic  of 
epitheliomata.  Often  these  pearls  are  large  enough  to  be  visible 
to  the  naked  eye.  (Pearls  are  also  occasionally  seen  in  papillo- 
mata,  ulcerative  processes  and  in  granulation  tissues  around  in- 
growing nails.)  The  stroma  is  usually  well  marked,  consisting 
of  fibrous  tissue. 


142 


GENERAL    PATHOLOGY 


Growth  is  usually  slow  and  sometimes  latent  for  years;  while 
malignant,  epitheliomata  are  less  so  than  glandular  earcinomata, 

and  metastasis  may  not  occur  for  years,  but  in  rare  instances 
has  occurred  in  the  first  year.     I  Fig.  50.) 

Rodent  ulcer  is  an  epithelioma  occurring  upon  the  upper  parr 
of  the  cheek.  Its  cells  are  polygonal  or  even  spindle-shaped  in- 
stead of  squamous,  and  are  arranged  in  anastomosing  columns. 
Pearls  are  not  found. 

These  and  other  growths   of  like   structure  have  been   called 


c^ 


Fig.    50.— Squamous   epithelioma,      a.    epithelial   masses;    b.   epithelial    pearls;    c,    connective 
tissue;    d,    capillary    blood   vessels.       (McFarland.) 

basal  cell  earcinomata,  because  the  cells  retain  their  resemblance 

to  those  of  the  basal  layer  of  the  rete  malpighii  from  which  they 
are  derived,  whereas  in  the  more  slowly  growing  skin  cancers 
the  cells  become  flat  and  squamous  in  appearance. 

The  molluscum  contagiosum  is  a  small,  soft  epithelioma,  found 
ofteriesl  ou  the  face,  arm-,  chesl  and  external  genitals,  and  usu- 
ally multiple.     It  consists  of  radial,  hyperplastic  columns  of  the 


TUMORS  143 

rete  malpighii,  with  degenerated  cells  in  the  center,  which  usu- 
ally show  granular  bodies,  believed  by  some  to  be  parasites. 

Adenocarcinomata 

Adenocarcinoma,  or  "malignant  adenoma,"  is  a  carcinoma 
resembling  the  glandular  tissue  from  which  it  springs.  Tliis 
tumor  arises  primarily  from  the  mucous  membranes,  especially 
of  the  stomach,  rectum,  uterus,  oviducts,  gall  bladder  and  bile 
ducts.  It  is  secondary  in  the  liver,  lymph  glands,  lungs,  kidneys, 
and  bones.  These  tumors  arc  more  apt  to  occur  in  the  young  than 
the  epitheliomata. 

Gross  Pathology. — Adenocarcinomata  are  usually  soft  and  on 
section  appear  gelatinous;  there  is  a  tendency  to  infiltrate  and 
tn  grow  outwardly  into  polypoid  masses.     (Fig.  51.) 

Pathologic  Histology. — Irregular  tubular  alveoli  are  seen,  lined 
with  columnar  cells  in  one  or  more  layers,  the  outer  layers  being 
the  more  typically  columnar.  The  alveoli  are  separated  by  fibrous 
or  mucoid  stroma.  In  later  stages  the  alveoli  are  filled  with 
various-shaped  epithelial  cells  and  the  tubular  character  may  be 
lust.  In  typical  eases  the  alveoli  are  not  solidly  filled  with  cells 
(at  least  all  the  alveoli  are  not  so  filled)  thus  distinguishing  these 
tumors  from  the  scirrhous  and  medullary  forms. 

Malignancy. — Adenocarcinomata  usually  grow  rapidly,  and 
metastasis  occurs  early. 

Scirrhous  Carcinoma 

Scirrhous  carcinoma  is  a  hard,  fibrous  tumor  found  most  fre- 
quently in  the  breast  (female),  uterus,  pylorus,  esophagus,  rec- 
tum, and  kidney. 

Gross  Pathology. — Scirrhous  cancer  is  a  hard,  round  or  irregu- 
lar tumor  adherent  to  the  overlying  skin  and  adjacent  tissues,  ex- 
cept in  very  early  stages.  By  contraction  of  the  fibrous  stroma, 
in  the  breasts,  it  causes  retraction  of  the  nipple,  and  irregulari- 
ties of  the  surface.  Section  shows  a  grayish  white,  glistening 
surface,  the  central  part  of  which  may  retract.  Yellow  areas 
of  fatty  tissue  are  often  seen  in  the  center  of  the  tumor.  It  is 
not  encapsulated,  the  periphery  being  the  more  vascular  part  of 
the  growth.  Sometimes  contraction  is  more  rapid  than  prolifera- 
tion, causing  the  atrophic  scirrhous  cancer.     (Fig.  52.) 


144 


GENERAL   PATHOLOGY 


Fig.  51. — Adenocarcinoma  of  the  body  of  the  uterus,  o,  may  be  likened  to  a  main 
stem  from  which  arise  numerous  secondary  stems,  which  in  turn  give  off  delicate  ter- 
minals, consisting  of  epithelial  cells.  The  glands  may  lie  divided  into  groups  a,  b,  c,  d,  and 
c,  by  the  stems  of  stroma  /,  g,  and  It.  The  stems  are  covered  by  several  layers  of  cylin- 
dric  epithelium,  while  projecting  into  the  gland  cavities  are  long  slender  ingrowths  of 
epithelium,  devoid  of  stroma,  as  seen  in  i.  Very  delicate  ingrowths  consisting  merely  of 
two  layers  of  epithelium  are  seen  at  k  and  k.  At  /  the  epithelium  is  several  layers  in 
thickness,  and  at  m  many  layers  with  leucocytes.  The  arborescent  character  of  the  growth 
and  peculiar  gland  grouping  are  characteristic  of  adenocarcinoma.      (Cullen.) 


TUMORS  145 

Pathologic  Histology.  Conspicuous  bands  of  fibrous  tissue 
form  alveoli,  enclosing  nests  of  epithelial  cells.  The  blood  ves- 
sels are  thick  and  fibrous.  The  alveoli  in  the  center  of  the  tumor 
are  smaller  than  toward  the  periphery,  and  the  cells  are  atrophied 
or  variously  degenerated. 

Secondary  involvement  of  the  lymphatic  glands  occurs  "within 
the  first  year. 

Medullary  Carcinoma 

Medullary  carcinoma  is  a  soft,  rapidly  growing,  brain-like 
tumor,  found  most   frequently  in  the  mammae  and  testes.    Secon- 


-   ■*■■***       -..'       '    -■  :  r- 


Fig.    52. — Scirrhous   carcinoma   of   breast.      Alveoli    of   epithelial    cells   small;    stroma   abun- 
dant.     (Mallory.) 

dary  tumors  of  this  type  may  follow  the  scirrhous  form.  Medul- 
lary cancer  occurs  somewhat  earlier  in  life  than  scirrhous,  but 
is  much  less  common  than  the  latter. 

Gross  Pathology. — This  tumor  is  soft  and  sometimes  fluctuat- 
ing, nodular  in  outline,  and  tending-  to  ulcerate  and  bleed  (fungus 
hematodes).  The  skin  adheres  early  and  retracts,  but  there  is 
no  retraction  of  the  nipple  when  the  breast  is  involved.  The 
tumor  is  fairly  well  circumscribed  owing  to  its  rapid  growth. 
(Fig.  53.) 


14G  GENERAL    PATHOLOGY 

Pathologic  Histology. — The  fibrous  stroma  is  more  or  less  em- 
bryonic, vascular  and  scant.  The  alveoli  are  Large  and  filled 
with  epithelial  cells  proliferating  rapidly,  sometimes  showing 
mitosis. 

These  tumors  are  usually  rapidly  fatal. 

Carcinoma  simplex  is  a  form  intermediate  between  the  scir- 
rhous and  the  medullary  forms  in  the  relative  proportion  of 
stroma,  cells,  and  vascularity. 

Melanocarcinoma  is  very  rare,  but  occurs  in  the  skin;  is  soft 
and  malignant. 

Adamantinoma   is   rare   occurring  on   the   surfaces   or  within 


i&t- 


Fig.    53. — Medullary   carcinoma   of   breast.      (Stengel   and    Fox.) 

the  substance  of  the  jaw  bone.  It  appears  to  be  derived  from 
the  enamel  of  developing  teeth,  and  consists  of  a  fibrillar  stroma 
surrounding  irregular  masses  of  epithelial  cells.  It  is  usually 
benign,  but  may  infiltrate  and  cause  atrophy  of  the  jaw,  and  some- 
times become  sarcomatous. 

Endotheliomata 

Endotheliomata  are  tumors  derived  from  endothelium  of  blood 
and  lymphatic  vessels,  also  the  nicsothelium  of  serous  membranes, 
and  hence  are  called  hemangioendotheliomata,  lymphangioendo- 
theliomata,  peritheliomata  (from  the  perivascular  lymph  spaces) 
and  mesotht  liomata. 


TiM(»i;s 


117 


In  addition  to  the  general  locations  mentioned,  they  occur  in 
the  meninges,  periosteum,  bone  marrow  and  other  parts.  While 
norma]  endothelial  cells  are  elongated  and  thin,  "forming  a  mo- 
saic over  the  surfaces  which  they  line,"  in  the  new  growths  the 
cells  become  cuboidal,  cylindrical,  and  irregular  in  shape.  They 
may  occur  in  tubular  masses,  or  in  several  layers  with  an  open 
lumen  here  ami  there,  or  in  solid  alveolar  masses  resembling 
carcinoma.      Pig.  54. 

A  psammoma  is  usually  an  endothelioma,  occurring  in  the 
meninges   ami    other   parts   of   the   brain,   consisting   of   closely 


■r 


Fig.  54. — Endothelioma  of  the  dura  mater.  a.  connective-tissue  stroma;  b,  small- 
ceiled  focus;  c,  proliferated  endothelium  from  lymph  vessels;  d,  endothelial  strand  with 
lumen;  c,  area  of  fatty  degeneration;  /,  endothelial  cells  passing  into  the  connective  tis- 
sue on  the   right.      (ZieglerJ 


packed  concentric  masses  of  cells  or  whorls.  They  contain  gran- 
ules of  calcareous  matter  i  "brain  sand").  Any  type  of  tumor  how- 
ever in  these  locations  containing  calcareous  granules  is  called 
a  psammoma. 

The  stroma  of  endotheliomata  may  become  hyaline,  myxoma- 
tous, fibrous  or  cartilaginous,  or  may  atrophy,  leaving  the  en- 
dothelium and  blood  vessels  as  the  main  features.  Such  tumors 
in  which  hyaline  or  mucoid  material  occurs  in  cylindrical  masses 
are  often  called  cylindromata. 

Endotheliomata  are  usually  benign. 


148  GENERAL   PATHOLOGY 

Teratomata 

Teratomata  are  tumors  of  complex  or  mixed  1  issues,  occurring 
in  abnormal  Locations,  and  due  to  developmental  misplacements 
of  tissues. 

They  are  said  to  be  endogenous,  when  superficial  tissues  have 
been  "included"  within  internal  parts,  and  ectogenous,  when  a 
part  of  one  fetus  has  been  included  within  another  fetus,  thus 
forming  the  point -of  origin  of  subsequent  tumor  formation.  In 
this  form  there  are  all  variations  and  amounts  of  inclusions  up 
to  double  monsters. 

Dermoid  Cysts 

Dermoid  cysts  are  teratoid  tumors,  characterized  by  the  pres- 
ence of  skin  or  one  or  more  of  its  appendages,  as  hair,  nails,  teeth, 
etc.    They  may  be  congenital  or  begin  to  form  late  in  life. 

Seats. — Dermoid  cysts  are  most  frequent  in  the  ovary,  but  also 
occur  in  the  testicle  and  oilier  organs.  They  are  apt  to  develop 
at  the  junction  of  fetal  clefts  and  fissures,  as  the  orbital  and 
mandibular  fissures,  branchial  clefts,  etc. 

Gross  Pathology. — The  growths  are  solid,  but  later  become 
cystic  by  retention  of  sebaceous  mailer,  sweat,  etc.,  which  gives 
them  a  putty-like  consistence.  They  are  round,  smooth  tumors, 
varying  in  size  up  to  that  of  a  child's  head. 

Microscopically,  tissues  of  the  three  blastodermic  layers  are 
present.  Skin  appears  in  patches  over  the  inner  surface  of  the 
cyst,  with  a  great  preponderance  of  sehaceous  glands.  Parts 
not  covered  by  skin  arc  usually  covered  by  mucous  membrane 
and  glands.  Besides  the  skin  appendages,  spicules  of  bone,  mus-- 
eh',  nerve  and  brain  tissue  may  be  seen. 

The  tumor  is  usually  benign,  but  may  become  carcinomatous. 

Hypernephroma 

Hypernephroma,  or  Grawitz's  tumor,  springs  from  a  portion  of 
the  suprarenal  cortex  include, I  within  the  kidney.  The  tumor  is 
a  yellow  new  growth  appearang  under  the  renal  capsule  in  the 
upper  portion  of  this  organ.  It  is  usually  small,  but  may  be- 
come large.  Histologically  there  are  found  epithelial  cells  ar- 
ranged in  tubules  as  in  the  cortex  of  the  suprarenal  capsules. 


TUMORS 


I  I!) 


No  medullary  cells  are  present,  hence  no  secretion  of  epinephrine 
has  been  found.     (Fig.  55.) 

Cholesteatoma  is  a  tumor  exhibiting  whitish  glistening  bodies 
of  concentric  layers  of  epithelioid  cells.  These  bodies  often  con- 
tain crystals  of  cholesterin.  The  tumor  occurs  in  the  brain  and 
meninges  and  is  often  multiple.  Hairs,  hair  follicles,  and  horny 
changes  have  been  found  in  these  tumors,  which  places  them 
among  the  teratomata. 

Chorionepithelioma,  or  syncytioma  malignum,  is  a  rapidly 
growing  tumor,  springing  from  the  placental  area  during-  preg- 


Fig.    55. — Finer    structure    of    the    adenomatous    form    of    hypernephroma. 

and  Fox  ) 


(After    Stengel 


nancy  or  the  puerperium.  The  tissue  resembles  placental  tissue. 
The  uterine  wall  is  rapidly  invaded  and  metastasis  occurs  to 
lungs  and  rarely  elsewhere.  The  tumor  has  no  blood  vessels  but 
grows  within  the  placental  spaces.     (Fig.  56.) 

Cysts 

Cysts  are  abnormal  collections  of  fluid  or  semifluid  materials 
within  a  closed,  sac-like  cavity. 

They  are  usually  classified  and  named  as  follows: 
1.  Retention  Cysts. — These  are  due  to  occlusion  of  the  excre- 
tory ducts  of  a  gland,  causing  distention  with  accumulating  se- 


150  GENERAL   PATHOLOGY 

cretions,  e.g.,  wens,  or  sebaceous  gland  cysts;  ranulce,  from  the 
salivary  or  mucous  glands  in  the  floor  of  the  mouth;  also  renal, 
ovarian,  parovarian,  mammary  and  pancreatic  cysts'.  An  entire 
organ  may  become  cystic,  as  the  kidney  in  hydronephrosis  (from 
an  occluded  ureter).     (Fig.  57.) 

2.  Softening'  or  Necrotic  Cysts. — These  are  due  to  degeneration 
and  liquefaction  necrosis  of  normal  or  pathologic  tissues,  and 
condensation  of  the  surrounding  tissue   into  a  limiting  area  or 


.Vjp- 


'*>>-• 


— "»■ ■  "».—.  "    "C  *■,'■*■       ,  -  •  -  .^  *- 

-'":'& 

f'  »  c©  ®*' 

..*  *'*■»•--».* 
■  'i     '*v»C~ » 

-••      -*  '^ 

■■,f :'*■''■■''  ■"■':" 
■  ■'■'■  \t£> 

Fig.  56. — Chorionepithelioma  or  syncytioma  malignum.  (By  tlie  courtesy  of  Dr.  Barton 
Cooke  Hirst  from  a   painting  made   for   him   from  a  slide   belonging   to   Dr.   Herbert  Fox.) 

wall.     They  occur  frequently  in  tumors,   infarcts,   etc.,  and   may 
follow  hemorrhages  (hemorrhagic  cysts). 

3.  Parasitic  Cysts. — Necrotic  softening  occurs,  irritation  causes 
the  formation  of  a  capsule,  and  the  liquid  contents  contain  epi- 
thelial debris  and  parasites.  Such  are  the  hydatid  cysts,  due  to 
the  tenia  echinococcus,  occurring  usually  in  the  liver,  less  often  else- 
where;  also  cysts  of  the  trichina  spiralis,  usually  of  small  size, 
just  visible  to  the  naked  eye,  and  occurring  within  the  muscle 
tissues. 

4.  Glandular  Cysts,  or  Cystomata. — These  are  adenomata, 
which  tend  to  cyst  formation.     They  occur  usually  in  the  ovary 


TUMOKS 


i  r,  i 


and  testicle,  but  may  be  found  in  any  glandular  tissue.  They 
may  be  single  or  multiple,  and  each  may  consist  of  one  or  many 
cavities  (multilocular  cysts).  They  vary  in  size  up  to  that  of  a 
child's  head  or  Larger.  On  section  a  more  or  less  serous,  some- 
times hemorrhagic  fluid,  or  a  gelatinous  material  (usually  re- 
ferred to  as  "colloid")    may   be   seen.     The   inner  surface   may 


Fig.  57. — Cyst  of  the  parovarium:     there  is  no  distortion  of  the  ovary;   the  Fallopian  tube 
has  been  much  elongated. 

be  smooth,  or  present  papillomatous  outgrowths  (papuliferous 
cysts  or  cystomata). 

Microscopically,  the  cysts  are  lined  with  typical,  or  variously 
modified,  columnar  epithelium,  supported  upon  a  framework  of 
connective  tissue.  The  latter  may  greatly  predominate,  causing 
the  cysts  to  be  very  small,  or  the  acini  few;  again  the  opposite 
may  be  true. 

Cysts  are  benign,  though  some  have  a  tendency  to  become  car- 
cinomatous. 


CHAPTER  VIII 

THE  PATHOLOGY  OF  INFECTIOUS  DISEASES 

An  Infectious  Disease  is  one  that  is  caused  by  living  micro- 
organisms. A  Contagious  Disease  is  an  infectious  disease  that  is 
readily  transmitted  from  one  individual  to  another  by  direct 
contact,  by  fomites,  etc. 

Any  organism  that  lives  upon  or  within  the  living  tissues  of 
plant  or  animal  is  called  a  parasite.  An  organism  which  lives 
upon  dead  and  decomposing  organic  matter  is  called  a  saprophyte. 
Those  parasites  or  saprophytes  which  can  live  and  flourish  in  either 
condition  are  known  as  facultative  or  optional  parasites  or  sa- 
prophytes. All  pathogenic  microorganisms  are  parasitic;  some 
are  habitual  parasites,  as  certain  pyococci,  the  B.  coli  communis, 
etc.,  while  other,  as  the  B.  tetani,  are  but  temporarily  parasitic. 
All  pathogenic  parasites,  which  can  be  grown  upon  artificial 
culture  media,  are  facultative  saprophytes. 

The  organisms  pathogenic  for  man  may  be  classified  as  fol- 
lows : 

Bacteria,   or   Schizonrycetes   (fission  fungi). 

Yeasts,  or  Blastomycetes  (budding  fungi). 

Molds,  or  Hyphomycetes  (thread  fungi). 

Protozoa,  or  unicellular  animal  microorganisms. 

Metazoa,  or  multicellular  animal  organisms. 

It  is  customary  to  refer  to  a  disease  caused  by  bacteria  or 
protozoa  as  an  infection;  to  one  caused  by  yeasts  as  a  blastomy- 
cosis; to  one  caused  by  molds  as  a  mycosis;  and  to  one  due  to 
metazoa  as  an  infestation. 

Bacteria  are  unicellular,  vegetable1  microorganisms,  which  re- 


1The  question  whether  bacteria  belong  to  the  vegetable  or  animal  kingdom  is  still 
an  open  one.  They  are  considered  plants  by  most  biologists  because  many  bacteria  can 
be  made  to  grow  upon  inorganic  food,  and  because  in  growth  and  reproduction  they 
resemble  plants  more  closely  than  animals,  bacteria,  however,  are  such  primitive  forms 
and  so  slightly  differentiated,  resembling  plants  in  rigidity  of  form,  in  tendency  to 
filamentous  growth  and  ability  of  some  of  them  to  grow  on  inorganic  food,  and  on 
the  other  hand  resembling  animals  in  motility,  lack  of  chlorophyl  and  apparent  neces- 
sity of  some  for  organic  food,  that  they  are  generally  regarded  as  occupying  a  place 
intermediate  between  the  plant  and  the  animal.  In  1878  Haeckel  proposed  that  bac- 
teria be  placed  in  a  separate  kingdom  to  be  known  as  Protista,  but  this  suggestion  was 
never  generally  accepted. 

152 


PATHOLOGY   OF   INFECTIOUS    DISEASES  153 

produce  by  fission.  Elongated  bacteria  (bacilli  and  spirilla)  di- 
vide transversely,  thus  differentiating  them  from  protozoa  which 
divide  longitudinally. 

Bacteria  are  divided  into  (a)  Lower  Bacteria  (Haplobacteria) — 
each  individual  organism  of  which  is  composed  of  a  single  cell, 
capable  of  performing  all  the  vital  essential  functions  and  (b) 
Higher  Bacteria  (Triehobacteria,  or  Trichomycetes) — composed 
of  filamentous  forms  (thread-like  arrangement  of  cells)  with  real 
or  apparent  branchings.  The  end-cells  only  appear  to  reproduce, 
hence  there  is  here  the  beginning  of  a  division  of  physiologic 
function. 

Bacteria  cause  disease  mainly  by  the  production  of  specific 
toxins;  i.e.,  poisonous  substances  secreted  by  the  bacteria,  and 
peculiar  (hence  "specific")  to  the  particular  organism  which  se- 
cretes them.  Toxins  resemble  enzymes  in  all  essential  properties, 
and  are  usually  divided  into  (a)  true,  soluble  or  extracellular 
toxins, — toxins  which  in  culture  media  escape  from  the  bacterial 
cell  (extracellular)  and  diffuse  through  the  medium  (soluble), 
and  (b)  intracellular,  endotoxins,  such  as  the  toxins  of  pyococci, 
the  typhoid  bacillus  and  most  of  the  pathogenic  bacteria — toxins 
which  remain  within  the  bacterial  cells  (intracellular)  and  are 
liberated  in  disease  when  the  bacterial  cells  disintegrate.  In 
addition  to  the  specific  toxins,  bacteria  may  also  form  various 
other  metabolic  products,  such  as  hemolysins,  coagulating,  pro- 
teolytic and  other  ferments,  as  well  as  various  nonspecific  and 
specific  substances. 

When  bacteria  with  their  toxic  products  gain  entrance  into 
the  blood  and  tissues,  they  stimulate  the  tissue  cells  to  the  pro- 
duction of  defensive  substances,  or  antibodies.  All  cells  or  sub- 
stances capable  of  causing  living  tissues  to  form  antibodies  are 
called  antigens.  The  most  important  antibodies  are  antitoxins, 
which  combine  with  and  neutralize  toxins,  thus  rendering  the  latter 
harmless;  agglutinins,  which  cause  bacteria  to  clump  together; 
Jgsins,  which  destroy  bacteria  and  other  cells;  and  opsonins,  which 
prepare  bacteria  in  some  manner  so  that  they  are  more  easily 
ingested  and  destroyed  by  the  phagocytic  leucocytes. 

Immunity  is  a  state  of  resistance  to  an  infection.  It  may  be 
actively  acquired  by  the  production  of  antibodies  during  the 
course  of  an  infection,  or  during  the  process  of  intentional  in- 


154  GENERAL   PATHOLOGY 

oculation,  as  in  "immunization"  in  which  animals  are  inoculated 
for  the  purpose  of  producing  antitoxic  and  bacteriolytic  sera,  or 
as  in  "vaccination"  or  "bacterination."  in  which  attenuated  or 
killed  cultures  of  bacteria  are  inoculated  into  healthy  persons  to 
cause  the  formation  of  antibodies  as  a  matter  of  protection  against 
infection,  or  into  diseased  individuals  for  the  purpose  of  effect- 
ing a  cure  of  the  disease.  Immunity  may  also  be  passively  ac- 
quired when  antitoxic  sera  ("antitoxins")  and  bacteriolytic  sera 
("antisera",),  manufactured  within  the  tissues  of  an  animal  or 
even  a  human  being,  are  injected  into  the  tissues  of  another  in- 
dividual for  the  purpose  of  protection  or  cure. 

Natural  immunity  is  not  well  understood,  but  may  be  defined 
as  that  which  is  possessed  by  an  individual  or  race,  not  known 
to  have  experienced  any  of  the  recognized  processes  of  protec- 
tion. 

A  septicemia  (or  bacteremia)  is  a  disease  due  to  the  presence 
of  bacteria  with  their  toxins  in  the  blood.  Thus  typhoid  fever, 
anthrax,  etc..  are  septicemias,  as  well  as  generalized  staphylococ- 
cic or  streptococcic  infection,  though  surgeons  are  apt  to  limit  the 
term  "septicemia"  to  invasion  of  the  blood  by  pyogenic  organ- 
isms. 

A  pyemia  is  a  condition  in  which  secondary  (metastatic)  ab- 
scesses appear  in  various  organs  and  tissues,  formed  by  bacterial 
emboli  brought  by  way  of  the  blood  vessels  or  lymphatic  vessels 
from  some  primary  focus  of  suppurative  inflammation. 

A  toxemia  is  a  diseased  condition  due  to  the  absorption  of  the 
toxins  of  pathogenic  bacteria,  as  in  tetanus. 

A  sapremia  is  a  condition  due  to  the  absorption  into  the  blood 
of  poisonous  substance  formed  by  saprophytic  bacteria  growing 
in  mortifying  tissues,  as  in  certain  forms  of  gangrene,  retained 
portions  of  placenta  after  parturition,  etc. 

SUPPURATIVE  DISEASES 

Suppuration  (q.v.)  or  inflammation  resulting  in  pus  formation, 
when  occurring  naturally,  is  always  the  result  of  the  invasion 
and  activity  of  microorganisms.  The  most  common  pyogenic  or- 
ganisms are  the  staphylococci  and  streptococci;  less  often  the 
pneumococci,  the  pneumobaeilli,  gonococci,  the  colon  and  typhoid 
bacilli;  still  less  commonly,  other  microorganisms,  including  ame- 


PATHOLOGY    OF    [NFECTIOUS    DISEASES  155 

bse,  may  become  pyogenic,  ruder  perfectly  favorable  conditions 
it  is  believed  thai  most,  if  no1  all,  pathogenic  bacteria  may  cause 
suppural  ion. 

The  micrococcus  tetragenus  and  the  />'.  pyocyaneus  are  often 
associated  with  the  more  common  pyococci  in  causing-  suppura- 
tion, the  latter  giving  a  green  tinge  to  the  pus,  but  they  rarely 
if  ever  arc  I  lie  sole  cause  from  the  beginning  to  the  end  of  the 
infection. 

The  staphylococcus  pyogenes  aureus  (cluster-forming,  pus-pro- 
ducing golden  yellow  spherical  organism)  is  the  direct  cause,  as 
a  rule,  of  localized  and  circumscribed  inflammation  and  suppura- 
tion, such  as  abscesses,  pustules,  furuncles,  carbuncles,  etc. 
"When  these  cocci  gain  entrance  into  the  circulation,  pyemia  and 
septicemia  may  result,  though  less  often  than  in  streptococcal  in- 
fection. The  organisms  may  remain  dormant  at  times  within 
an  encapsulated  inactive  abscess,  or  in  deeply  seated  subacute 
infections,  as  in  subacute  osteomyelitis,  endocarditis,  etc.,  and 
later  become  active  and  virulent.  The  presence  of  staphylococci 
in  association  (symbiosis)  with  other  organisms  in  disease  often 
aids  the  activity  of  the  latter,  as  for  example  the  influenza  bacilli. 

Their  specific  toxins  are  intracellular,  and  have  a  decided  chemo- 
tactic  effect  upon  the  leucocytes,  attracting  large  numbers  of 
these  phagocytes  to  the  seat  of  infection.  A  hemolytic  substance 
is  also  formed.  Although  staphylococci  cause  the  formation  of 
antibodies,  the  use  of  antistreptococcic  sera  has  not  been  very  en- 
couraging, but  the  use  of  vaccines  of  killed  or  attenuated  cul- 
tures has  been  more  promising,  especially  in  subacute  or  chronic 
staphylococcic  infections. 

The  staphylococcus  pyogenes  cilbus,  and  the  staphylococcus  epi- 
dermic] is  alb  us  are  mildly  pathogenic  forms,  probably  but  slightly 
modified  varieties  of  the  S.  pyogenes  aureus.  The  first  is  often 
associated  with  the  aureus  variety  in  suppurations,  or  may  be 
the  sole  cause  in  certain  forms  of  acne.  The  latter  inhabits  the 
layers  of  the  epiderm,  and  in  the  opinion  of  some  bacteriologists 
is  the  cause  of  "stitch  abscesses." 

The  Streptococcus  pyogenes  (chain-forming,  pus-producing  coc- 
cus) varies  considerably  in  virulence,  but  usually  causes  the 
more  severe  forms  of  suppurative  disease,  with  a  tendency  to 
spread  and  become  phlegmonous.     Cellulitis,   erysipelas,  perios- 


156  GENERAL   PATHOLOGY 

titis,  pleuritis,  peritonitis,  etc.,  as  also  general  septicemia,  are 
more  often  due  to  streptococci  than  to  staphylococci.  Strep- 
tococci are,  however,  also  found  in  localized  suppurations.  In 
malignant  endocarditis  the  Streptococcus  viridans,  a  variety  form- 
ing green  colonies  on  culture  media,  is  commonly  found.  In  rheu- 
matic arthritis  the  Streptococcus  rheumaticus  is  apparently  the 
chief  exciting  cause.  In  erysipelas  the  Streptococcus  erysipelatis 
is  found,  but  this  appears  to  be  identical  with,  the  Streptococcus 
pyogenes.  Erysipelas,  (literally  "red  skin")  is  a  serous  inflam- 
mation of  the  skin,  usually  found  on  the  face,  tending  to  spread 
from  the  nose  outward  across  the  cheeks,  and  preceded  by  a  zone 
of  congestion  and  dense  infiltration  which  follows  the  lymphatic 
clefts.     Occasionally  suppuration  occurs. 

Streptococci  are  often  found  in  the  throat  and  tonsils  during 
infectious  diseases,  such  as  measles,  scarlatina,  influenza,  etc. 

Kosenow  believes  that  streptococci  and  pneumococci  are 
merely  different  varieties  of  one  species  and  has  apparently  suc- 
ceeded in  transmuting  one  to  the  other  variety  under  artificial 
conditions. 

In  regard  to  toxins,  antibodies,  and  vaccines,  what  was  said 
of  the  staphylococci  is  also  true  in  general  of  the  streptococci. 

Epidemic  Cerebrospinal  Meningitis 

Epidemic  cerebrospinal  meningitis  is  a  purulent  inflammation  of 
the  cerebral  and  spinal  meninges,  caused  by  the  meningococcus, 
or  Diplococeus  intracellularis  meningitidis.  These  cocci  occur  in 
pairs,  and  resemble  the  gonococci  both  in  morphology  and  in 
being  found  in  groups  within  the  leucocytes  and  other  cells.  They 
also  sometimes  occur  in  chains. 

The  disease  is  a  fibrinopurulent,  less  often  a  seropurulent  lep- 
tomeningitis, the  cerebral  dura  being  rarely  involved,  although 
the  spinal  dura  is  often  involved.  The  exudate  is  abundant  in 
the  large  fissures  of  the  brain,  over  the  optic  chiasm  and  sur- 
faces of  the  pons  and  the  cerebellum.  The  inflammation  usually 
follows  the  blood  and  lymph  vessels  into  the  substance  of  the 
brain  and  cord,  often  resulting  in  small  abscesses.  The  fluid 
from  a  lumbar  puncture  nearly  always  contains  the  cocci,  and 
the  cocci  have  frecpiently  been  found  in  the  nasal  secretions  of 
patients  and  of  persons  exposed  to  the  disease.     It  is  believed 


PATHOLOGY    OP    INFECTIOUS   DISEASES  157 

that  meningeal  invasion  occurs  by  way  of  the  lymphatic  vessels 
from  the  nose. 

Various  inflammations  and  degenerations  are  also  noted  in  the 
kidneys,  heart,  spleen,  muscles,  and  other  tissues. 

Gonorrhea 

Gonorrhea  is  a  purulent,  catarrhal  inflammation  of  the  urethra 
and  other  mucous  membranes,  caused  by  the  gonococcus  or  Mi- 
crococcus gonorrheae.  This  organism  occurs  in  pairs,  "biscuit- 
shaped"  or  "coffee-bean-shaped"  in  appearance,  and  found 
abundantly  in  the  pus  of  acute  gonorrhea  of  the  urethra,  less 
often  in  chronic  cases,  or  in  other  locations.  In  acute  gonor- 
rheal urethritis  the  inflammation  begins  at  the  meatus  and  soon 
spreads  to  the  posterior  parts;  the  mucosa  is  intensely  red,  and 
in  about  twenty-four  hours  or  more  a  yellowish  (sometimes 
greenish)  exudate  appears,  consisting  of  leucocytes  and  des- 
quamated epithelium.  Microscopical  examination  shows  groups 
of  the  gonocoeci  lying  within  the  pus  cells,  as  well  as  in  the  fluid 
portion  of  the  exudate. 

From  the  original  focus,  other  tissues  are  readily  invaded, 
causing  salpingitis,  oophoritis,  peritonitis,  prostatitis,  also  me- 
tastasis to  more  remote  tissues,  as  the  heart  and  the  joints  (gonor- 
rheal endocarditis  and  arthritis).  "Gonorrheal  rheumatism" 
usually  occurs  months  after  the  infection,  is  very  intractable  and 
apt  to  result  in  permanent  damage  to  the  joint,  usually  the  knee, 
elbow  or  wrist. 

Ophthalmia  neonatorum  is  an  acute  gonorrheal  conjunctivitis 
contracted  by  the  child  from  the  mother  during  parturition.  It 
is  said  that  10  per  cent  of  blindness  in  children  is  due  to  this 
form  of  gonorrhea. 

Chronic  gonorrhea  is  usually  a  direct  continuation  of  an  acute 
attack,  and  characterized  by  a  constant  discharge  of  a  thin, 
catarrhal  exudate  (gleet).  Ulcerous  lesions,  or  papillomatous 
thickenings  of  the  mucosa  are  a  frequent  result  of  chronic  gonor- 
rhea, or  there  may  be  hyperplasia  of  the  submucosal  connective 
tissue  with  narrowing  of  the  urethra  (stricture).  The  most  com- 
mon seat  of  stricture  is  the  membranous  urethra. 


158 


GENERAL    PATHOLOGY 


The  gonotoxin  is  intracellular,  and  while  slight  amounts  of 
antibodies  are  produced,  antisera  are  valueless,  but  vaccines  may 
be  useful  in  chronic  forms  of  the  disease. 

"While  gonorrhea  is  usually  contracted  through  sexual  contact, 
the  transmission  of  the  disease  by  towels,  bedding,  and  other 
contaminated  articles,  particularly  in  institutions,  is  probably 
more  frequent  that  is  generally  recognized.  Latent  gonorrheal 
foci,  existing  long  periods  of  time  after  apparent  "cures"  have 
been  effected,  and  capable  of  becoming  acute  and  transmitting 


Fig.    58. — Acute   urethritis,    showing   purulent    infiltration   and    gonococci    in    the    cells    and 
between    the    cells.       (Birch-Hirschfeld.) 

the  disease  to  others,  are  also  more  frequent  than  is  generally 
believed.     (Fig.  58.) 


Soft  Chancre,  or  Chancroid 

Soft  chancre,  or  chancroid,  is  an  ulcer  almost  invariably  found 
on  the  external  genitals,  due  to  the  B.  of  Ducrey.  It  is  always 
contracted  through  sexual  contact,  but  is  autoinocnlable,  hence 
there  are  usually  more  than  one  ulcer.  The  infection  begins  as  a 
red  papule,  which  later  suppurates,  forming  a  yellowish  ulcer 
with  irregular  infiltrated  margins.    Sometimes  it  becomes  phage- 


PATHOLOGY   OF    [NFECTIOUS    DISEASES  159 

denic  or  serpiginous  in  character.  The  organisms  travel  along 
the  lymphatic  channels  to  the  inguinal  glands  which  also  sup- 
purate as  a  rule.  The  disease  is  purely  local — never  systemic 
when  uncomplicated.  Mixed  infection  often  occurs,  and  gono- 
eocci.  Spirochete  pallida,  pyogenic  cocci,  and  other  organisms  may 
be  found  in  the  ulcers. 

Pneumonia,  or  Pneumonitis 

Pneumonia  is  an  inflammation  of  the  essential  lung  tissue;  viz.. 
the  alveoli  and  their  immediately  surrounding  structures.  The 
clinical  forms  of  pneumonia  are  practically  always  due  to  micro- 
organisms, but  many  different  species  of  the  latter  have  been 
found  as  the  direct  cause  of  the  disease,  and  it  is  possible,  more- 
over, to  produce  a  pneumonia  by  the  inhalation  of  hot  steam 
or  chemical  irritants.  Pneumonia,  therefore,  should  be  con- 
sidered as  a  distinct  pathologic  condition  rather  than  a  specific 
infection.  Classified  according  to  their  pathologic  anatomy,  pneu- 
monias may  be  divided  into: 

Lobar,  Fibrinous  or  Croupous  Pneumonia. 
Lobular.  Catarrhal  or  Bronchopneumonia. 
Purulent  or  Suppurative  Pneumonia. 
Fibroid,  Interstitial  or  Productive  Pneumonia. 
Tuberculous  or  Caseous  Pneumonia. 

Lobar,  or  Croupous,  Pneumonia  is  an  acute  hemorrhagic  and 
exudative  inflammation  of  the  air  cells  of  one  or  more  lobes  of 
the  lungs,  due  usually  to  the  pneumococcus,  or  Diplococcus  pneu- 
moniae,  but  occasionally  to  streptococci,  staphylococci,  B.  influ- 
enza?, the  B.  of  Friedlander.  and  other  organisms,  either  alone 
or  in  association  (symbiosis  I  with  the  pneumococcus. 

Cold,  fatigue  and  systemic  depression  of  any  nature  act  as  pre- 
disposing causes.  The  lover  right  lobe  is  oftenest  affected;  next 
the  lower  left  lobe,  and  rarely  the  apices.  In  "double  pneu- 
monia" lobes  in  both  sides  of  the  thorax  are  simultaneously  in- 
volved. 

There  are  three  principal  stages: 

(a)  Congestion. — The  diseased  area  is  hyperemic,  dark  red.  less 
crepitant  than  normal,  heavy  but  still  floating  when  placed  in 
water,  and  the  pleural  surfaces  are  lustreless.  Microscopically, 
the  capillaries  are  congested,  and  the  air  cells  contain  a  serous 


160 


GENERAL    PATHOLOGY 


exudate  with  red  and  white  blood  cells,  and  a  few  desquamated 
epithelial  cells.  As  this  exudate  increases  in  amount,  coagulation 
sets  in  (few  hours  to  a  few  days)  thus  forming  the 

(b)  Stage  of  Consolidation  or  Hepatization. — The  affected  area 
is  now  solid  and  liver-like,  deep  red  or  brownish  red  in  color 
(red  hepatization),  is  swollen,  pits  on  pressure  and  sinks  when 
placed  in  water.  On  section  the  cut  surface  is  red,  dry,  and 
granular — due  to  plugs  of  fibrin  projecting  from  the  air  cells. 
A  fairly  thick  slice  of  the  diseased  lobe  will  break  on  bending. 
Microscopically  the  air  vesicles  are  filled  with  fibrin  holding  in  its 


Fig.  59. — Acute  lobar  pneumonia.  Early  stage.  This  single  air  vesicle  shows  conges- 
tion of  the  capillaries  in  the  walls,  and  a  small  amount  of  exudates,  fibrin,  leucocytes, 
red  blood  cells,  and  exfoliated  epithelium.      (Delafield  and   Prudden.) 


meshes  red  and  white  cells  and  desquamated  epithelium.  The 
fibrin  soon  begins  to  contract  causing  a  serous  fluid  to  collect 
in  the  vesicles,  the  red  cells  disintegrate,  the  epithelial  cells  be- 
come fatty,  and  when  these  changes  have  advanced  far  enough 
to  give  the  affected  areas  a  yellow  or  grayish  color,  the  name 
"gray  hepatization"  is  applied.  The  area  is  still  solid  but  less 
apt  to  break  on  bending,  and  the  air  cells  contain  a  mass  of  fibrin 
which  is  retracted  from  the  walls  and  cells,  chiefly  leucocytes  and 
epithelium.  (Figs.  59  and  60.)  This  substage  (gray  hepatiza- 
tion) does  not  always  develop — the  red  hepatization  passing  at 
once  into  the  third  stage  of 

(c)  Resolution. — The  affected  area  now  softens,  pitting  is  no 


PATHOLOGY    OF    [NFECTIOUS   DISEASES 


161 


Longer  possible  and  crepitation  can  again  be  elicited.  On  section 
a  purulent  fluid  exudes. 

Microscopic/I! //,  liquefaction  necrosis,  Avitli  cells  in  different 
stages  of  disintegration  are  the  chief  features.  Proliferation  of 
epithelial  cells  becomes  marked,  thus  repairing  the  damaged  al- 
veolar -walls,  -while  the  softened,  emulsified  contents  are  being 
absorbed  by  the  lymphatics  and  in  part  expectorated. 

During  the  course  of  the  disease,  the  lung  tissues  surrounding 
the  inflamed  parts  are  more  or  less  emphysematous,  and  the  pleura 
is  usually  inflamed,  hence  a  typical  pneumonia  is  nearly  always  a 


Fig.  60. — Acute  lobar  pneumonia.  Later  stage.  The  air  vesicles  are  filled  with  exu- 
date consisting  of  leucocytes,  fibrin,  and  serum  with  a  few  epithelium  cells.  (Delafield 
and  Prudden.) 

pleuropneumonia.  A  blood  examination  shows  leucocytosis. 
Rarely,  in  intense  intoxications  a  leucopenia  is  present.  Paren- 
chymatous changes  in  the  kidneys  and  heart  may  occur  due  to 
the  toxemia ;  albuminuria  is  frequent,  and  the  chlorides  are  di- 
minished or  absent  from  the  urine  during  the  disease,  but  usually 
reappear  in  excess  during  convalescence. 


Bronchopneumonia  or  Lobular  Pneumonia 

Bronchopneumonia  or  lobular  pneumonia  is  an  acute  inflamma- 
tion starting  in  the  smaller  bronchioles  and  extending  to  the  air 
cells  of  the  lungs,  in  which  the  exudate  shows  little  or  no  ten- 
dencv  to  fibrin  formation.    About  one-half  of  the  lobular  forms 


162 


GENERAL   PATHOLOGY 


of  pneumonia  are  due  to  the  pneumococcus,  either  alone  or  as- 
sociated with  the  organisms  mentioned  under  croupous  pneu- 
monia. Any  of  the  organisms  mentioned  may  also  be  the  sole 
cause  of  this  form  of  pneumonia. 

Bronchopneumonia  is  most  frequent  in  the  young  and  the  aged, 
and  may  be  secondary  to  measles,  whooping  cough,  scarlatina, 
diphtheria,  pulmonary  cirrhosis,  typhoid  fever,  etc. 

Grossly  the  pleural  surface  presents  red  or  grayish  areas,  which 
correspond  to  the  lobules  or  areas  of  the  terminal  bronchioles 
affected.     In  extensive  cases  all  the  lobes  of  both  lungs  may  be 


Fig.  61. — Bronchopneumonia.  Child.  The  wall  of  the  small  bronchus  is 
and  the  lumen  contains  a  mucopurulent  exudate.  The  adjacent  air  vesicles 
tain  a   catarrhal   exudate.      (Delafield   and   Prudden.) 


thickened 

also  con- 


involved,  but  not  all  the  lobules  are  affected,  i.e.,  the  lobes  are 
not  uniformly  affected  as  in  lobar  pneumonia.  The  inflamed, 
lobular  areas  usually  project  slightly  above  the  surrounding  sur- 
faces, and  are  surrounded  by  emphysematous  tissue.  The  lung  as 
a  whole  is  crepitant,  but  the  localized  diseased  areas  are  airless 
and  sink  in  water.  The  bronchi  and  bronchioles  contain  muco- 
purulent exudates,  and  their  complete  obstruction  sometimes  leads 
to  local  areas  of  atelectasis.     (Fig.  61.) 

Microscopically  the  alveoli  are  filled  with  a  semifluid  exudate 
containing  desquamated  epithelium  and  blood  cells.  The  alveolar 
walls  show  round-cell  infiltration  and  the  bronchioles  catarrhal 
bronchitis. 


PATHOLOGY    OF    [NFECTIOUS    DISEASES  163 

Hypostatic  pneumonia  is  ;i  bronchopneumonia,  not  so  distinctly 
lobular  as  the  ordinary  form,  and  with  an  exudate  thai  is  more 
fibrinous.  It  commonly  involves  the  bases  and  posterior  (de- 
pendent)  parts  of  the  Lungs  in  individuals  who  are  confined  to 
bed  during  prostrating  diseases,  as  typhoid  or  chronic  nephritis. 
When  the  heart  action  becomes  feeble  hypostatic  congestion  de- 
velops in  the  dependent  parts  and  soon  bacteria  enter  the  con- 
gested part  and  set  up  a  catarrhal  inflammation. 

Aspiration  pneumonia  is  also  a  form  of  bronchopneumonia  re- 
sulting from  the  inspiration  of  infectious  material  from  the  upper 
air  passages,  as  well  as  food  and  secretions  from  the  mouth  in 
eases  of  paralysis,  in  anesthesia,  or  from  the  inhalation  of  hot 
steam,  chemical  irritants  or  dust  in  concentrated  form.  The  le- 
sions vary  with  the  causal  factors.  When  infectious  or  highly 
irritating  matter  is  "aspirated,"  an  intense  catarrhal  inflamma- 
tion with  solidification  results;  the  exudate  is  hemorrhagic  and 
liable  to  become  suppurative  or  necrotic.  In  the  inhalation  of 
dust,  as  in  marble  cutting,  coal  mining,  etc.,  the  catarrhal  inflam- 
mation may  be  moderate  in  degree  or  absent,  while  the  produc- 
tive inflammation,  with  a  resulting  fibroid  pneumonia,  may  be  the 
main  pathologic  change. 

Purulent  pneumonia  is  an  acute  inflammation  in  which  pyogenic 
bacteria,  whether  as  a  secondary  infection  brought  by  way  of 
the  bronchi,  blood  channels  or  the  pleura,  or  as  a  primary  in- 
fection, cause  suppuration  of  the  inflammatory  exudate.  Small 
miliary  abscesses,  or  one  or  more  large  abscesses  may  result,  a 
condition  which  is  very  apt  to  be  fatal.  When  the  abscesses 
break  into  the  pleural  cavity,  an  empyema  results.  The  term, 
empyema,  refers  to  a  collection  of  pus  in  the  pleural  cavity  how- 
ever produced. 

Fibroid  pneumonia  is  a  chronic  process  in  which  the  cellular 
proliferation  becomes  permanent  fibrous  tissue.  When  this  con- 
dition is  caused  by  the  inhalation  of  coal  dust,  iron  dust,  or 
marble  dust  (pneumonokoniosis)  the  particles  penetrate  the  al- 
veolar walls  and  the  walls  of  the  bronchioles,  and  become  sur- 
rounded by  a  zone  of  inflammatory  exudate  which  finally  or- 
ganizes into  fibrous  tissue.  This  form  of  pneumonia  also  occurs 
at  times  secondary  to  other  forms  of  pneumonia,  to  syphilis,  tu- 
berculosis, etc.     When  the  indurated  areas  are  extensive,  con- 


164  GENERAL   PATHOLOGY 

traction  with  distortion  of  the  lung  follows,  with  obliteration 
of  the  air  cells  and  proportionate  impairment  of  respiration. 

Caseous  or  tuberculous  pneumonia  is  due  to  the  B.  tuberculosis, 
and  characterized  by  a  filling  up  of  the  air  cells  and  an  infiltration 
of  the  interalveolar  tissues  with  an  exudate  which  tends  to 
caseation  instead  of  resolution.  There  are  small  areas  of  con- 
solidation, usually  lobular,  at  first  red  (congestion),  later  yellow 
(caseation).  These  areas  finally  soften  and  undergo  resolution, 
if  small,  or  become  encapsulated,  or  may  coalesce  into  larger 
cavities,  resulting  in  chronic  pulmonary  tuberculosis;  if  mixed 
infection  occurs,  rapid  suppurative  softening  results  and  the  con- 
dition quickly  becomes  fatal  ("galloping  consumption.") 

The  specific  or  infectious  granulomata  are  smaller  or  larger 
masses  of  pathologic  tissue,  resulting  from  subacute  or  chronic 
proliferative  inflammatory  processes,  due  to  specific  microor- 
ganisms, and  having  a  tendency  toward  degenerative  or  necrotic 
change.  The  lesions  are  for  the  most  part  tubercles,  nodules  or 
nodes,  consisting  essentially  of  more  or  less  typical  granulation 
tissue,  but  there  is  no  tumor  in  the  true  sense,  and  the  term 
"granuloma"  is  deservedly  falling  into  disuse. 

The  lesions  usually  described  under  this  heading  are  those 
found  in  tuberculosis,  leprosy,  glanders,  syphilis,  rhinoscleroma, 
actinomycosis,  sporotrichosis,  blastomycosis,  etc. 

In  the  following  pages  the  pathology  of  the  lower  or  true 
bacterial  diseases  will  be  considered  immediately,  while  those 
morbid  conditions  due  to  the  higher  bacteria  and  other  organisms 
will  be  taken  up  in  their  proper  order. 

Tuberculosis 

Tuberculosis  is  a  disease  comprising  the  morbid  processes  due 
to  the  B.  tuberculosis.  It  affects  man  and  practically  all  the  lower 
animals,  though  goats,  horses,  dogs,  and  cats  are  relatively  im- 
mune. 

Locations. — It  is  found  in  the  respiratory  tract,  the  gastroin- 
testinal tract  (especially  the  lower  ileum,  rectum,  throat  and 
mouth),  the  lymph  nodes,  serous  membranes,  bones,  spleen,  kid- 
neys, adrenals,  brain,  middle  ear,  uterus  with  appendages,  tes- 
ticles, bladder,  and  skin.     Organs  which  are  rarely  affected  are 


I'ATIlOUHiY    OF    IXKKCTIOCS    DISEASES 


165 


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Fig.    62. — Miliary   tubercles   in   the   liver,   showing  abundant   round   cells   in   the   peripheral 
pails,  epithelioid  and  giant-cells  within.      (Stengel  and  Fox.) 


Fig.  63. — Miliary  tubercle  of  the  human  form.      (Stengel  and  Fox.) 


166  GENERAL   PATHOLOGY 

the  salivary  glands,  thyroid  gland,  the  muscles,  cartilages,  ovaries 
and  heart. 

In  children  the  lymph  nodes,  serous  membranes  and  the  bones 
are  most  frequently  infected. 

Gross  Pathology. — The  characteristic  lesion  is  the  miliary  tu- 
bercle. This  is  a  gray,  semitranslucent,  slightly  elevated  (if  su- 
perficially located)  nodule  varying  in  size  from  a  point  scarcely 
visible  to  the  naked  eye  to  2  mm.,  which  merges  into  the  sur- 
rounding tissue  (can  not  be  "peeled  out").  The  second  form  of 
tuberculous  lesion  is  an  infiltration  of  the  tissues  with  epithelioid 
cells  and  other  cells  characteristic  of  the  tuberculous  process,  but 
without  forming  distinct  tubercles.  When  caseation  sets  in,  the 
lesions  become  yellow  (yellow  miliary  tubercle).  (Figs.  62  and 
63.) 

Minute  Anatomy. — The  bacilli  (or  their  toxins)  first  cause  pro- 
liferation of  the  endothelial  cells  of  the  lymph  spaces,  lymph 
capillaries  and  blood  vessels  and  connective  tissue  of  the  part. 
These  cells  are  large  and  have  vesicular,  poorly  staining  nuclei, 
and  known  as  epithelioid  cells.  Giant  cells  (large  multinucleated 
cells)  may  appear  in  the  midst  of  the  epithelioid  cells,  probably 
formed  from  the  latter  by  proliferation  of  the  nuclei  without  di- 
vision of  the  cytoplasm.  Round  cells,  consisting  of  leucocytes 
and  lymphocytes,  surround  the  collection  of  epithelioid  cells,  and 
at  this  stage  it  may  be  possible  at  times  to  see  the  three  zones 
usually  described  as  consisting  of  an  inner  zone  of  giant  cells, 
a  middle  zone  of  epithelioid  cells  and  an  outer  zone  of  round 
cells.  This  is  the  histology  of  the  gray  tubercle ;  no  new  blood 
vessels  are  formed,  and  after  a  variable  time,  the  center  becomes 
cheesy  (cheesy  necrosis),  the  cells  lose  their  outline  and  the 
nuclei  degenerate,  giving  the  field  a  granular  appearance,  which, 
surrounded  by  cells  not  yet  having  undergone  degeneration, 
presents  the  so-called  "raked  field"  appearance.  The  giant  cells 
also  degenerate,  and  those  which  have  undergone  but  partial 
degeneration  have  a  crescentic  outline.  Giant  cells  are  not  neces- 
sarily present,  but  are  characteristic  of  a  typical  tubercle. 

The  histologic  appearance  of  tuberculous  infiltration  is  essen- 
tially the  same,  but  there  are  more  blood  vessels  in  the  area,  and 
especially  upon  free  surfaces  a  typical,  highly  vascular  granula- 
tion tissue  may  be  formed. 


PATHOLOGY    OF    [NFECTIOUS   DISEASES  1 07 

Results.  When  well  established,  the  disease  progresses  usu- 
ally to  a  fatal  termination.  Many  times,  however,  caseation  may 
be  followed  by  encapsulation  with  temporary  arrest  of  the  in- 
fectious process  (latent  foci),  or  by  calcification,  and  if  the  dis- 
ease has  nol  progressed  too  far,  a  permanent  cure  is  possible. 
When  the  lesions  undergo  liquefaction,  cavities  (vomica;)  are 
formed,  or,  especially  in  cases  of  bone  infection,  cold  abscesses 
result. 

Secondary  tuberculosis  may  be  set  up  in  various  parts  of  the 
body  by  (1)  extension  along  lymphatic  channels,  (2)  along  nat- 
ural channels,  as  the  respiratory  or  intestinal  tract,  and  (3) 
through  the  blood  vessels. 

Leprosy 

Leprosy  is  a  chronic  infectious  disease  due  to  the  B.  lepra. 

It  occurs  in  two  forms,  the  nodular  (or  tubercular)  and  the 
anesthetic.  In  the  first,  gray  or  yellowish  nodules  develop,  vary- 
ing in  size  up  to  a  walnut,  or  larger.  (Fig.  64.)  These  occur  in 
the  skin  and  subcutaneous  tissues  of  the  face,  exterior  surfaces 
of  the  legs  and  arms,  about  the  hands  and  other  parts,  and  are 
red  and  inflammatory  at  first,  but  later  pale  and  indolent.  They 
usually  break  down  into  ulcers  which  slowly  cicatrize,  often  Avith 
great  distortion.  The  mucous  membrane  and  internal  organs  may 
also  rarely  be  affected. 

In  the  anesthetic  form  the  lesions  are  less  conspicuous,  but  the 
hyperesthesia,  neuralgia  and  later  atrophic  ulcers  make  it  more 
serious  than  the  nodular  form.  Anesthesia  of  the  parts  occurs 
when  the  ulcerations  develop. 

The  two  forms  are  often  associated,  and  tuberculosis  often  fol- 
lows the  lesions,  especially  those  of  the  internal  organs. 

Microscopically,  the  nodule  is  seen  to  be  fibrous,  somewhat  vas- 
cular without  tendency  toward  caseation.  It  is  composed  of 
epithelioid  cells  (proliferated  endothelium  and  connective  tissue 
cells)  which  are  often  vacuolated  and  may  contain  the  bacilli; 
large  degenerated  cells  ("lepra  cells")  containing  many  bacilli 
and  a  few  more  or  less  degenerated  nuclei  are  always  found. 
Giant  cells  are  sometimes  present,  but  far  less  often  than  in  tu- 
berculosis. 


1G8 


GENERAL    PATHOLOGY 


In  the  anesthetic  form  the  bacilli  grow  within  the  sheaths  of 
nerves,  forming  fusiform  swellings,  resembling  the  nodules  in 
structure. 

Skin  eruptions  (pemphigus  leprosa)  often  occur,  also  atrophy 
of  the  parts  affected,  and  sometimes  even  loss  of  parts,  as  fingers 
or  toes. 


Fig.   C4. — Xodular  leprosy.     (Goldschmidt.) 


Syphilis,  or  Lues  (or  "Great  Pox") 

Syphilis  is  an  infectious  disease  due  to  the  presence  of  the 
Spirochete  pallida,  or  Treponema  pallidum.2  It  occurs  in  three 
stages. 


2There  is  a  tendency  to  place  this  organism  among  the  protozoa.  It  is  a  rigid  spiral,  in 
many  respects  resembling  the  spirilla,  but  it  is  claimed  by  some  observers  that  in 
reproduction  longitudinal  division  takes  place,  which  would  place  the  spirochete  among 
the  animal  organisms.  According  to  Jordan  {General  Bacteriology,  1918),  "At  present  the 
systematic  position  of  this  organism  may  be  regarded  as  unsettled,  although  the  majority 
of  investigators  incline  to  place  it  with  the  true  bacteria,  or  at  best  in  a  group  midway 
between   the   bacteria   and    protozoa.'' 


PATHOLOGY    OF    [NFECTIOUS    DISEASES  169 

The  primary  stagi  Is  characterized  by  the  chancre,  which  appears 
after  an  incubation  period  of  three  weeks,  a1  the  site  of  u 
lation,  as  a  red  papule  increasing  in  size  and  hardness  (Hunte- 
li.-ni  chancre).  It  usually  presents  a  dry,  sometimes  slimy  super- 
ficial erosion,  but  docs  not  ulcerate;  is  located  usually  upon  the 
glans  penis,  prepuce,  or  just  within  the  meatus;  in  the  female,  in 
the  vagina,  urethra  or  cervix  uteri.  Extragenital  chancres  may 
occur  in  the  rectum,  about  the  anus,  in  the  mouth,  eyes,  groin 
ami  other  locations. 

Wherever  the  initial  lesion  occurs,  local  lymphadenitis  devel- 
ops simultaneously,  forming  the  "indolent  bubo" — painless, 
hard  and  movable  beneath  the  skin. 

Histologically,  the  chancre  consists  of  round  cell  infiltration 
leucocytes  and  proliferated  connective  tissue  cells)  within  the 
deeper  layers  of  the  skin  or  mucous  membrane,  and  especially 
along  the  course  of  the  blood  vessels.  There  is  considerable  in- 
tercellular exudate,  which  coagulates,  favoring*  necrosis  of  the 
superficial  cells  (erosion). 

The  chancre  attains  a  maximum  size  in  one  to  two  weeks,  from 
a  few  millimeters  to  a  few  centimeters  in  diameter,  remains  sta- 
tionary for  three  or  four  weeks,  then  slowly  disappears,  though 
the  induration  may  persist  for  years. 

The  secondary  stage  may  follow  in  about  six  weeks,  and  is 
characterized  by  eruptions  upon  the  skin  and  mucous  mem- 
branes, with  swelling  and  induration  of  the  lymphatic  glands 
generally.  The  eruptions  begin  as  papules  or  macules  which  be- 
come flat  tabular  swellings  with  superficial  erosion,  having  a  dull 
red  or  coppery  color  on  the  skin,  and  a  grayish  color  on  the  mu- 
cous membrane  the  mucous  patch).  These  eruptions  are  poly- 
morphous in  outline,  are  covered  with  a  scant  secretion,  often 
offensive,  sensitive  to  the  touch,  and  the  most  contagious  of 
syphilitic   lesions. 

Histologically,  there  is  round  cell  infiltration,  with  edema  and 
necrosis  of  the  epithelium.  The  papilla  become  abnormally  large 
and  hyperemic. 

These  eruptions  last  from  one  to  three  years,  then  disappear, 
and  recovery  may  lie  effected,  or  the  tertiary  stage  may  follow. 

The  tertiary  stage  may  follow  the  secondary  in  from  one  to  four 
years,  or  after  many  years,  and  is  characterized  by  the  presence 


170  GENERAL   PATHOLOGY 

of  gummata,  which  are  nodules  varying  in  size  from  a  pinhead  to 
an  orange.  They  occur  most  frequently  in  bones,  especially  tibia, 
sternum  and  skull;  in  internal  organs,  as  liver,  kidneys,  lungs, 
brain  and  other  parts. 

^lacroscopically,  a  gumma  is  a  hard,  somewhat  elastic  nodule ; 
on  section  the  central  part  is  found  to  be  gelatinous  in  appearance. 
Fibrous  bands  are  usually  seen  radiating  from  the  center  to  the 
periphery  and  into  the  surrounding  tissues.  Tin-  hard  and  elastic 
character  suggested  the  name  "gumma,"  i.e.,  gummy  tumor.  The 
center  may  soften,  especially  when  near  a  surface,  forming  ulcers 
which  finally  cicatrize.    (Fig.  65.) 


3: 


m 


Fig.   65.  —Gummatous  meningoencephalitis.      (Ziegler.) 

Histologically,  the  gumma  is  composed  of  round  and  spindle 
cells  and  usually  a  few  giant  cells.  The  blood  vessels  are  markedly 
thickened,  and  new  vessels  are  formed.  Degeneration  or  a  form 
of  necrosis  (resembling  caseation)  is  always  seen  in  the  center  of 
the  gumma. 

There  are  also  diffuse  tertiary  syphilitic  lesions,  such  as  bands 
of  connective  tissue,  greatly  thickened,  atheromatous  vessel  vails, 
with  a  diffuse  infiltration  of  tissues  with  the  characteristic  round 
cells;  often  seen  in  the  liver,  spleen,  kidney,  heart,  and  nervous 
system. 


PATHOLOGY    OF    INFECTIOUS    DISEAI  171 

Glanders,  or  Equinia 

Glanders  is  an  acute1  or  chronic  infectious  disease,  occurring 
spontaneously  in  horses,  due  to  the  B.  mallei,  and  occasionally 
communicated  to  man  and  other  animals. 

In  horses,  the  nasal  mucosa  is  the  usual  seat  of  inoculation,  in 
which  slightly  elevated,  pea-sized  nodules  appear,  which  increase 
and  finally  break  down,  leaving'  yellowish  ragged-edged,  pus-dis- 
charging ulcers.  When  these  heal,  characteristic,  stellate  scars 
are  formed.  Bronchopneumonia  by  aspiration  of  infected  mate- 
rials from  the  nose  or  upper  air  passages  may  follow.  Metastatic 
abscesses  of  internal  organs  often  occur.  The  disease  is  often  fatal, 
death  occurring  with  all  the  symptoms  of  a  septicemia. 

When  the  skin  is  particularly  involved,  the  condition  is  called 
farcy  and  the  nodules  in  the  skin  and  subcutaneous  tissues,  vary- 
ing in  size  up  to  hazelnuts,  are  called  f<irvij  buds.  These  also 
tend  to  suppurate.  Farcy  is  more  frequently  chronic  in  its  course 
than  is  the  nasal  form,  or  glanders  proper. 

In  man,  the  lesions  are  essentially  similar  to  those  occurring  in 
the  horse,  but  the  disease  is  usually  an  acute,  febrile,  septicemic 
affection  and  usually  fatal,  though  in  the  rarer  chronic  form,  50 
per  cent  are  said  to  recover.  Infection  occurs  through  the  nose, 
conjunctiva,   and  abrasions  of  the  skin. 

Histologically,  the  nodules  consist  of  dense  masses  of  small 
round  cells  of  lymphoid  type  together  with  leucocytes  and  epi- 
thelioid cells  at  the  periphery.  AVhen  suppuration  occurs  these 
cells  degenerate  and  become  pus  cells.  Chronic  glanders  (rare 
in  man)  is  characterized  by  slowly  extending  ulcers  with  scar 
formation. 

Rhinoscleroma  (literally,  a  hard  tumor  of  the  nose)  is  a 
chronic  infectious  disease,  characterized  by  the  formation  of 
small,  hard  nodules  in  the  skin  of  the  anterior  nares  and  upper 
lip,  with  a  tendency  to  spread  over  the  face  or  into  mouth  and 
pharynx,  observed  most  frequently  in  Europe,  rarely  elsewhere, 
and  due  to  the  B.  rhino scleromatis,  a  bacillus  practically  identical 
in  morphology  and  cultural  characteristics  with  B.  of  Fricdlander 
(pneumobacillus) . 


172  GENERAL   PATHOLOGY 

THE  TOXEMIC  DISEASES 

All  pathogenic  microorganisms  form  toxins,  but  a  few,  such  as 
the  B.  tetani,  the  B.  diphtheria?  and  the  spirillum  of  Asiatic  chol- 
era form  true,  soluble  toxins,  which  are  so  highly  poisonous,  that 
these  organisms  may  be  regarded  as  preeminently  toxieogenic, 
and  the  diseases  produced  as  true  toxemias. 

Tetanus  or  Lock  Jaw 

Tetanus  is  an  infectious  disease  characterized  by  an  intense  in- 
toxication, due  to  the  B.  tetani. 

The  tetanus  bacillus  is  a  spore-forming,  anaerobic  organism. 
It  will  not  grow  in  presence  of  air  in  culture  media  or  in  the  tis- 
sues. Infection  therefore  occurs  usually  through  deeply  pene- 
trating wounds,  or  when  aerobic  organisms  are  carried  into 
the  wound  together  with  Hie  tetanus  bacillus  or  its  spores,  or 
when  there  is  considerable  injury  to  the  tissues.  Such  conditions 
favor  the  anaerobic  requirements  of  the  bacillus;  wounds  which 
do  not  fulfill  these  conditions  are  not  apt  to  develop  the  infection 
even  when  inoculated.  The  tetanus  bacillus  is  a  saprophyte  in 
the  soil,  particularly  garden  earth,  manure,  and  dust,  and  a  para- 
site in  the  intestines  of  herbivorous  animals. 

The  local  reaction  of  the  bacillus,  apart  from  the  inflammation 
caused  by  associated  organisms,  is  usually  very  insignificant. 
After  an  incubation  period  of  nine  days  (few  days  to  several 
weeks)  stiffness  of  the  jaw  and  neck,  or  spasms  of  the  muscles 
about  the  infected  wound  develop.  Tonic  spasms  of  these  parts 
soon  follow,  and  later  general  tonic  and  clonic  convulsions 
develop  and  continue  until  death  results  from  exhaustion  or  as- 
phyxia (spasm  of  the  glottis),  or  until  recovery  takes  place. 
These  symptoms  are  all  due  to  irritation  of  the  motor  cells  of  the 
cord  and  brain  by  the  toxin,  which  travels  along  the  nerve  tracts 
from  the  infected  wound  to  the  central  nervous  system. 

Antitetanic  serum  (antitoxin)  is  curative,  but  must  be  used  in 
time  to  combine  with  the  toxin  before  the  latter  has  reached  the 
motor  cells.  Since  the  first  symptoms  are  usually  evident  only 
when  the  toxin  has  reached  the  cord,  the  use  of  the  serum  fre- 
quently fails.  Its  most  successful  use  is  that  of  a  preventive  in 
cases  where  inoculation  was  thought  probable. 


PATHOLOGY    OF    [NPECTIOl  S    DISEASES  I?.'! 

Diphtheria 

Diphtheria  is  an  acute  infectious  inflammation  duo  to  />'.  diph- 
theriae  (Klebs-Loeffler  bacillus),  and  characterized  by  the  forma- 
tion of  a  false  membrane  locally,  and  by  toxemia  systemically. 

While  the  tonsils,  pharynx  and  the  nose  are  the  common  seats  of 
the  disease,  the  eyes,  skin,  middle  ear,  vagina,  and  other  parts  may 
also  become  infected.  Symbiosis  with  streptococci  increases  the 
virulence  of  the  diphtheritic  bacillus.  After  an  incubation  of  from 
2  to  7  days,  an  acute  fibrinous  inflammation  sets  in,  the  exudate  of 
which  as  it  appears  upon  the  surface  undergoes  coagulation  necro- 
sis, thus  forming  a  thick,  adherent  membrane — the  false  or  diph- 
theritic membrane.  In  the  larynx  this  membrane  with  the  swollen 
and  inflamed  mucosa  may  cause  fatal  asphyxia,  but  aside  from  this 
purely  mechanical  condition,  diphtheria  becomes  serious  or  fatal 
only  through  the  toxin  which  is  formed.  The  bacilli  rarely  invade 
the  blood  or  internal  organs.  At  necropsy  are  found  degeneration 
and  inflammation  of  the  myocardium  and  endocardium,  and  ne- 
phritis. Bronchopneumonia  is  present  in  over  50  per  cent  of  fatal 
cases,  due  to  B.  diphtheriae,  to  pneumococci  or  other  organisms. 

During  convalescence  paralysis  of  the  soft  palate  and  other  mus- 
cles often  occurs. 

The  use  of  antidiphtheritic  serum  (antitoxin)  affords  the  best 
example  of  successful  serotherapy  in  the  art  of  therapeutics. 

Asiatic  Cholera 

Asiatic  cholera  is  an  acute  infectious  disease  characterized  by 
a  serous  inflammation  of  the  intestines  and  due  to  the  Spirillum 
or  Vibrio  cholerae  asiaticae,  often  called  the  "comma  bacillus"  of 
Koch. 

The  spirilla  invade  the  mucosa  of  the  lower  part  of  the  ileum 
chiefly,  also  often  the  large  bowel,  causing  an  intense  watery  exuda- 
tion, which  with  the  contained  particles  of  desquamated  epithelium, 
constitutes  the  "rice-water"  discharges,  so  prominent  a  symptom 
of  this  disease.  Postmortem  examination  reveals  no  definite  or 
constant  morbid  changes,  but  often  congestion  or  inflammation  are 
noted  in  the  affected  parts,  with  degenerative  changes  in  the  liver, 
kidneys,  and  other  organs.  The  spirilla  do  not  enter  the  blood, 
but  secrete  a  soluble  toxin,  which  either  alone  or  together  with  other 
toxic  products  accounts  for  the  symptoms. 


174  GENERAL   PATHOLOGY 

Typhoid  Fever 

Typhoid  fever  is  an  acute  general  infection  of  the  lymphade- 
noid  tissue  of  the  body,  with  its  most  characteristic  lesions  in  the 
lymphoid  structures  of  the  intestine,  and  due  to  B.  typhosus  (B. 
typhi  abdominalis)  of  Eberth.  The  bacilli  appear  in  the  blood  (a 
bouillon  culture  inoculated  with  blood  during  the  first  week  of  the 
disease  is  the  most  positive  means  of  diagnosis)  and  in  all  the  se- 
cretions and  excretions,  as  well  as  in  the  "rose  spots"  which  oc- 
cur upon  the  exterior  early  in  the  infection. 

As  in  Asiatic  cholera,  the  organisms  are  usually  ingested  with 
food  and  water.  After  an  incubation  period  of  two  or  three 
weeks,  the  solitary  follicles  and  Peyer's  patches  in  the  lower 
part  of  the  ileum  become  congested;  during  the  second  week 
these  become  pale  and  enlarged,  due  to  proliferation  of  the  lymph- 
oid cells  and  to  phagocytic  endothelial  cells  (macrophages) 
and  softening  and  necrosis  are  apt  to  take  place,  which  during 
the  third  week  results  in  ulceration.  When  the  Peyer's  patches 
ulcerate,  the  ulcers  are  longitudinally  disposed  with  reference 
to  the  long  axis  of  the  intestine  (thus  differing  from  the  tubercu- 
lous ulcer  in  the  same  situation  which  is  transverse).  After  the 
third  or  fourth  week  the  ulcers  begin  to  heal.-  Not  all  the  lymph 
follicles  or  patches  proceed  to  ulceration,  and  in  some  cases  no 
ulcers  are  formed  at  all.  In  some  cases  the  lymphoid  structures 
of  the  upper  colon  and  upper  ileum  are  also  involved.  On  the 
other  hand  the  intestinal  structures  may  not  be  involved,  the  in- 
fection electing  lymphoid  tissues  elsewhere  in  the  body  as  the 
seat  of  its  activity.  In  typical  typhoid  fever,  however,  the  in- 
testinal glands,  the  mesenteric  glands,  the  spleen,  liver,  kidneys, 
bone  marrow,  and  the  lymphoid  structures  in  other  parts  are  in- 
volved, showing  congestion,  cellular  infiltration,  and  frequently 
necrotic  areas.  The  spleen  is  greatly  enlarged  (splenic  tumor) 
in  nearly  all  cases. 

The  specific  toxin  is  an  endotoxin,  to  which  the  symptoms  of 
temperature,  delirium,  prostration  and  anatomic  changes  are  due. 
Agglutinins  are  also  formed,  and  their  presence  after  the  first 
week  of  the  disease  may  be  shown  by  the  Widal  reaction;  viz.. 
the  clumping  of  the  typhoid  bacilli  from  a  young  culture  when 
mixed   with    a   minute    quantity    of    the   patient's   blood   serum. 


PATHOLOGY    OF    IXFI'.CTIOI  -    DISKASKS 


175 


Antisera  are  of  qo  avail  therapeutically,  but  vaccination  lias 
proved  successful  as  a  preventive  measure. 

After  recovery,  the  organisms  continue  to  grow  in  the  liver 
and  oilier  parts  of  individuals,  as  well  as  in  a  few  persons  who 
never  had  the  disease  in  recognizable  form  (subinfection).  Such 
individuals  may  in  feet  others,  hence  are  called  "typhoid  car- 
riers." Diphtheria  and  a  number  of  other  infections  may  also 
be  ''carried"  for  variable  periods  of  time.     (Fig.  66.) 

Paratyphoid  infect  ion  is  a  mild  (rarely  fatal)  form  which  is 
clinically  almost  identical  with  typhoid  fever,  but  with  certain 
pathologic    differences,    and    due    to    "paratyphoid"    bacilli,    of 


Fig.    66. — Typhoid    fever,   showing    necrosis    of   Peyer's  patches   and    intense    congestion   of 
the  bowel.      (Modified  from  Kast  and  Rumpel.) 


which  there  are  several  strains,  and  which  differ  from  the  B. 
typhosus  in  certain  cultural  characteristics  and  in  agglutinative 
reactions. 

Bacillary  Dysentery 

Bacillary  dysentery  is  an  infectious  colitis  due  to  B.  dysen- 
teriae  (Shiga),  a  nonmotile  member  of  the  typhoid-colon  group. 
It  produces  toxins  which  are  probably  both  intracellular  and  ex- 
tracellular. Great  swelling  of  the  mucosa  of  the  colon  with  muco- 
catarrhal  inflammation  are  noted,  and  the  surface  of  the  colon 
becomes  considerably  eroded.  In  severe  cases  the  inflammation 
becomes  hemorrhagic  and  even  necrotic,  the  alvine  discharges 
varying  in  character  with  that  of  the  inflammation. 


176  GENERAL   PATHOLOGY 

Malta  Fever  or  Mediterranean  Fever 

Malta  fever  is  a  specific  infectious  disease,  clinically  resembling 
typhoid  fever,  and  characterized  pathologically  by  swelling  of 
lymphoid  structures,  as  Fever's  patches,  spleen,  etc.,  and  with 
ulcerative  inflammation  of  the  large  bowel,  and  due  to  the  Micro- 
coccus melitensis.  It  is  conveyed  by  means  of  the  milk  of  infected 
goats,  and  probably  in  other  ways.  The  disease  is  practically  un- 
known in  this  country. 

Anthrax 

Anthrax  is  an  infectious  disease  due  to  the  B.  anthracis,  occur- 
ring in  cattle  and  sheep  (splenic  fever)  and  communicated  to  man, 
in  whom  it  is  known  as  malignant  pustuU  and  wool  sorters'  dis- 
ease. 

Inoculation  of  the  skin  causes  an  intense  local  inflammation, 
consisting  of  a  rapid  infiltration  of  the  part  with  leucocytes,  great 
edema  and  large  numbers  of  the  bacilli.  Pustules  form  which  dis- 
charge a  bloody  fluid  and  become  covered  with  crusts.  The  pus- 
tules or  ulcers  are  intractable  owing  to  rapid  invasion  of  surround- 
ing tissues  by  the  bacilli,  which  also  enter  the  blood  stream,  and 
always  cause  a  hemorrhagic  splenitis.  Any  internal  organ  may  be 
involved  in  the  general  infection. 

When  inhaled,  as  in  wool  sorters'  disease,  a  severe,  atypical  lobu- 
lar pneumonia  results,  usually  with  involvement  of  the  mediastinal 
tissues,  endocarditis  and  pleurisy. 

A  typical  case  of  anthrax  presents  the  most  conspicuous  example 
of  septicemia  or  bacteremia  (more  specifically  in  this  connection, 
a  bacillemia)  to  be  found  in  the  study  of  infectious  disease.  Im- 
mense numbers  of  anthrax  bacilli  occur  in  the  circulation,  clogging 
the  capillaries  of  organs  and  tissues,  and  apparently  giving  weight 
to  the  early  theory  that  death  was  due  to  internal  asphyxiation. 
Moreover  no  toxin,  extracellular  or  intracellular,  has  been  dem- 
onstrated. It  is  probable,  however,  that  these  bacilli,  as  all  other 
pathogenic  bacteria,  form  some  kind  of  toxic  substance,  since  death 
has  occurred  in  some  anthrax  infections  in  the  absence  of  large 
numbers  of  the  bacilli  in  the  blood  vessels.  Antisera  have  proved 
successful  in  some  cases,  while  vaccination  of  cattle  has  been  uni- 
formly successful  as  an  immunizing  measure. 


PATHOLOGY   OF    [NFECTIOUS   DISEASES  177 

Malignant  Edema 

Malignant  edema  is  an  intense  infection  due  to  the  B.  edematis 
maligni  (Koch),  characterized  by  rapid  edematous  swelling-  of  the 
subcutaneous  tissues  with  suppuration  and  frequently  necrosis. 
The  organism  is  anaerobic  and  does  nol  enter  the  blood  stream. 
Infection  occurs  through  traumatisms,  and  is  rare. 

Gaseous  Edema 

Gaseous  edema  or  infectious  emphysema  is  an  infection  due  to 
the  B.  aerogenes  capsulatus  (Welch).  It  causes  an  edema  of  the 
tissues  with  gas  formation  at  the  area  of  inoculation,  usually  the 
subcutaneous  tissues.  The  whole  body  may  be  invaded.  Rapid 
necrosis  is  apt  to  follow.  Postmortem  examination  shows  gas  bub- 
bles in  the  internal  organs  and  in  the  blood,  rendering  this  fluid 
foamy.  Infection  takes  place  through  abrasions  of  the  skin  or 
traumatisms,  as  compound  fractures.  The  infection  is  very  grave, 
but  fortunately  not  very  frequent.  Postmortem  gaseous  edema 
takes  place  by  invasion  of  the  tissues  from  the  intestinal  tract,  in 
which  the  bacillus  is  found  as  a  parasite. 

Bubonic  Plague 

Bubonic  plague  is  a  general  infection  due  to  the  B.  pestis.  The 
disease  is  common  in  the  rat,  ground-squirrel  and  other  rodents, 
and  transmitted  to  man  by  the  rat  flea  and  probably  other  insects. 
There  are  three  forms  of  the  disease:  (a)  the  bubonic  form,  in 
which  polyadenitis  is  the  conspicuous  feature.  The  bacilli  are 
carried  from  the  seat  of  inoculation  to  the  nearest  lymphatic  glands 
which  become  swollen  and  inflamed  (primary  buboes).  From  these 
the  bacilli  are  carried  by  the  blood  stream  to  the  glands  of  the 
body  generally  (secondary  buboes).  There  is  a  great  tendency  to 
capillary  hemorrhage  into  the  surrounding  tissues,  due  to  the 
action  of  the  toxin  upon  the  capillary  walls,  setting  up  an  intense 
hemorrhagic  inflammation  (periadenitis).  The  glands  are  greatly 
swollen,  red  and  hemorrhagic;  later  they  soften  and  suppurate. 
Microscopically  the  blood  vessels  are  congested,  inflamed  and  their 
lumen  often  plugged  with  bacilli.  The  lymphoid  and  endothelial 
cells  are  proliferated  and  the  bacilli  fill  the  lymph  sinuses. 


178  GENERAL   PATHOLOGY 

(b)  The  pneumonic  form  may  result  from  the  bubonic  form  or 
be  directly  contracted  through  inhalation  of  the  virus  from  an- 
other diseased  individual.  A  lobular  form  of  pneumonia  results, 
attended  with  marked  edema  and  hemorrhages  into  the  lung  tissue. 
There  is  a  mucopurulent  bronchitis,  and  the  peribronchial  lymph 
glands  are  involved.  This  is  the  most  fatal  form  of  plague,  as  well 
as  the  most  contagious. 

(c)  The  septicemic  form  is  commonly  the  terminal  condition  of 
the  bubonic  and  pneumonic  forms,  but  at  times  plague  septicemia 
occurs  without  distinct  buboes  or  marked  inflammation  of  the 
glandular  tissues. 

In  all  forms  the  liver,  kidneys,  spleen  and  bone  marrow  are 
usually  congested  and  enlarged,  and  show  areas  of  hemorrhage, 
necrotic  foci  and  the  presence  of  the  bacilli. 

The  toxin  is  apparently  intracellular.  The  use  of  antisera  and 
of  prophylactic  vaccines  has  been  more  or  less  successful. 

Influenza 

Influenza  is  an  infectious  disease,  often  occurring  in  epidemics, 
less  often  in  pandemics  and  characterized  by  inflammation  of 
the  respiratory  tract,  gastrointestinal  tract,  meninges  and  other 
parts.     The  exudate  is  mucopurulent,  and  often  bloody. 

In  1892  Pfeiffer  found  in  the  blood  and  sputum  of  influenza 
patients  a  very  small  bacillus,  which  was  named  the  B.  influenzal 
and  regarded  as  the  specific  cause  of  the  disease.  But  the  recent 
pandemic  (1918-1919)  has  failed  to  confirm  this  view,  the  ma- 
jority of  investigators  apparently  believing  that  the  B.  influenzae 
is  merely  an  associated  organism  or  secondary  invader  of  the  tis- 
sues. This  bacillus  is  found  in  a  majority  of  uncomplicated  cases 
of  influenza,  and  in  the  secondary  pneumonia,  endocarditis,  otitis 
media,  meningitis,  etc.,  as  well  as  in  the  blood. 

Pneumonia  is  the  most  frequent  complication,  and  is  usually  an 
atypical  and  bilateral  bronchopneumonia,  of  a  more  or  less  hemor- 
rhagic type.  In  some  cases  the  areas  involved  are  lobar  rather 
than  lobular  in  extent.  The  B.  influenza?,  pneumococci  and  strep- 
tococci, either  alone  or  in  association,  are  the  chief  causal  factors 
of  the  pneumonia. 


PATHOLOGY    OF    [NPECTIOUS  DISEASES  179 

Epidemic  Conjunctivitis 

Epidemic  conjunctivitis  ("pink  eye")  is  a.  catarrhal  or  muco- 
purulent inflammation  of  the  conjunctivae,  due  to  the  Koch- 
Weeks  bacillus,  which  resembles  the  B.  influenza  in  morphology 
and  staining  reaction. 

Whooping  Cough  or  Pertussis 

Whooping  cough  is  a  specific  infectious  inflammation  of  the 
upper  air  passages,  occurring  usually  in  childhood  and  character- 
ized by  a  paroxysmal,  convulsive  cough.  A  short  oval  bacillus 
Mas  discovered  in  the  bronchial  exudate  by  Bordet  and  Gengou, 
and  named  B.  pertussis.  Later  the  organism  was  found  in  great 
numbers  lying  between  the  cilia  of  the  tracheal  and  bronchial 
epithelium.  It  can  be  found  in  large  numbers  in  the  early  stages 
of  the  disease,  but  later  other  organisms,  especially  the  influenza 
bacillus,  outgrow  it.  Bronchopneumonia  is  a  frequent  complica- 
tion of  pertussis,  and  tuberculosis  a  moderately  frequent  sequela. 

Vincent's  Angina 

Vincent's  angina  is  an  acute  infectious  inflammation  of  the 
tonsils,  spreading  to  the  pharynx,  characterized  by  superficial 
ulceration  and  pseudomembrane  formation,  due  to  an  anaerobic 
organism  which  in  the  early  stage  of  its  life  history  is  a  spindle- 
shaped  bacillus  (B.  fusiform  is)  and  later  becomes  a  spiral  form 
(Spirochuta  vincenti)  both  forms  appearing  in  the  exudate  and 
in  artificial  cultures. 

Relapsing  Fever 

Relapsing  fever  is  a  specific  infectious  disease,  due  to  the  Spiro- 
chuta obcrmcicri,  and  characterized  by  a  peculiar  febrile  course; 
viz.,  three  or  four  periods  of  five  to  seven  days  each  of  high  tem- 
perature, separated  by  periods  of  equal  length,  in  which  the  tem- 
perature is  normal  or  subnormal. 

The  spirochete  is  usually  classed  among  the  flagellated  protozoa, 
but  Novy  and  Knapp  have  demonstrated  that  it  has  many  of  the 
characteristics  of  bacteria,  and  its  classification  must  at  present  be 
considered  as  undetermined. 


180  GENERAL   PATHOLOGY 

The  spleen  and  lymphatic  glands  are  enlarged  and  often  the 
seat  of  various  forms  of  degeneration  or  necrosis.  The  organisms 
occur  abundantly  in  the  blood,  and  were  discovered  by  Obermeier 
in  1873. 

THE  HIGHER  BACTERIA 

( Trichomycetes,   Chalamy dobacteriacese ) 

These  are  filamentous  forms  (see  page  153)  which  are  inter- 
medial e  between  the  true  bacteria  and  the  molds.  Great  confu- 
sion prevails  in  the  classification  and  nomenclature  of  the  organ- 
isms, but  the  following  varieties  are  usually  recognized: 
Leptothrix — thread-like  filaments,  showing  no  branching  forms. 
Cladothrix — thread-like  filaments,  showing  false  branching  forms. 
Nocardia  (Streptothrix)  filaments,  showing  true  branching  forms. 
Actinomyces — radial   filaments,   showing    true   branching   forms. 

The  Nocardia  form  spores,  which  usually  appear  in  chains;  the 
actinomyces  are  further  characterized  by  formation  of  club- 
shaped  ends  at  the  periphery  of  the  rosette-like  colony,  and  by 
the  absence  of  spore-formation. 

The  bacilli  causing  tuberculosis,  diphtheria  and  glanders  some- 
times exhibit  branching  forms,  and  are  believed  by  many  to  be- 
long to  the  higher  bacteria. 

Leptothrix  Infections,  (Leptotrichoses) 

The  common  saprophyte  of  the  mouth  (L.  buccal  is)  may  accord- 
ing to  some  observers  become  pathogenic  and  form  white  patches 
on  the  tonsils  and  other  parts  of  the  mouth.  The  organisms  are 
regarded,  however,  by  most  pathologists  as  merely  associated  or- 
ganisms or  secondary  invaders. 

Cladothrix  and  Nocardia  Infections  or  Mycoses 

The  difference  between  true  and  false  branching  has  not  been 
definitely  established;  false  branching  being  merely  an  apparent 
branching  due  to  the  fact  that  portions  of  fragmented  filaments 
assume  the  position  of  branches  to  the  main  stem;  hence  all  that 
can  be  stated  definitely  at  present  is  that  organisms  belonging  to 
one  or  the  other  of  these  groups  have  been  found  in  a  causal 
relation  in  abscesses  of  the  brain,  in  lesions  of  the  lungs  resem- 


PATHOLOGY    OF    INFECTIOUS    DISEASES 


1*1 


bling  tuberculosis  very  closely,  and  in  other  Locations.  Mos1  ob- 
servers, however,  are  inclined  to  regard  the  pathogenic  forms  as 
belonging  to  the  Mocardia  (or  Streptothrices),  while  the  Clado- 
thrices  are  believed  to  be  harmless  saprophytes. 

Actinomycosis 

This  is  a  chronic  infectious  disease  due  to  the  Actinomyces 
bovis.  In  cattle  the  lower  jaw  is  principally  affected  ("lumpy 
jaw"),  less  frequently  the  upper  jaw,  tissues  of  the  neck,  the 
tongue  ("wooden  tongue")  and  rarely  other  parts.  In  man  the 
disease  occurs  occasionally,  affecting  the  mouth,  lungs,  and  ab- 
dominal  organs. 

The  invasion  of  the  organism  results  in  the  formation  of  a  hard 
nodule  which  slowly  increases  in  size  and  infiltrates  and  destroys 


Fig.  67. — Actinomycosis  of  the  tongue,     a.  actinomyces  granule;   b  and  c,  cellular  nodules; 
d,   transverse    section   of   muscle;    <•   and  /,    connective    tissue.      (Ziegler.) 

adjacent  tissues,  whether  these  be  soft  tissues  or  hone.  In  the  lungs 
the  lesions  often  resemble  tuberculosis.  Microscopically  there  are 
round  cell  infiltration,  proliferation  of  connective  tissue  cells  and 
formation  of  granulation  tissue  rich  in  leucocytes.  Occasionally 
giant  cells  appear.  Later  suppuration  and  necrosis  result.  Some- 
times repair  processes  proceed  in  one  portion  of  the  affected  area 
while  softening  advances  in  another,  causing  considerable  dis- 
figurement. 

Diagnostically  the  essential  feature  is  the  presence  of  the  para- 
site itself,  which  is  visible  to  the  naked  eye  as  a  gray  or  yellow 
"sulphur  granule."  These  granules  crushed  between  two  glass 
slides  are  seen  to  be  composed  of  one  or  more  rosettes  made  up  of 


182 


GENERAL   PATHOLOGY 


radially  disposed  filaments  ("ray  fungus")  with  club-shaped 
bodies  at  the  periphery,  and  usually  coccoid  in  the  center,  which 
may  be  degeneration  products  or  contaminating  cocci.     (Fig.  67.) 

Mycetoma,  or  Madura  Foot  of  India 

Mycetoma,  or  madura  foot  of  India,  is  due  to  the  Actinomyces 
madurse,  which  grows  upon  certain  thorns  whose  prick  causes 
the  development  of  slowly  growing,  marble-like  hard  nodules  on 
the  foot,  or  rarely  upon  the  hand.     These  nodules  suppurate  in 


Fig.    68. — Blastomycosis.      Old    partially    healed    ulcer    of    the    leg.      (Irons    and    Graham.) 

one  or  two  years,  the  pus  containing  white,  black   ("melanoid 
form")  or  rarely  red  granules. 

Blastomycosis  or  Saccharomycosis 

Blastomycosis  is  an  infection  caused  by  yeasts  (blastomycetes) , 
a  generic  term  for  fungi  which  reproduce  by  budding.  These  cells 
are  oval  or  spherical  (1-40/x)  and  nucleated.  Only  a  few  yeasts 
appear  to  be  pathogenic.  The  first  fatal  blastomycosis,  reported 
in  1894,  showed  an  ulcerous  inflammation  of  the  tibia,  with  metas- 
tasis to  the  internal  organs  and  the  lymph  glands.    A  number  of 


PATHOLOGY   OF   INFECTIOUS   DISEASES  183 

cases  of  blastomycetie  dermatitis  have  been  observed;  they  begin 
as  papules  which  ulcerate  and  spread,  and  run  a  chronic  and 
usually  fatal  course.     (Fig.  68.) 

Oidiomycosis 

Oidiomycosis  is  an  extremely  fatal  disease,  so  far  observed 
eh  icily  in  the  San  Joaquin  Valley,  California.  It  was  at  first 
thought  to  he  due  to  protozoa,  and  called  coccidioidal  granuloma, 
but  is  now  known  to  be  due  to  an  organism  resembling  both  yeasts 
and  molds.  Small  tumor-like  growths  are  formed,  followed  by 
fatal  generalized  infection  in  most  instances. 

Thrush,  or  Soor,  is  a  fungus  growth  found  in  the  mouth,  es- 
pecially of  bottle-fed  infants.  White  patches,  composed  of  the 
organisms  and  epithelial  debris,  form  on  the  palate  and  other 
parts.  The  causal  organism — oidium  albicans — grows  on  all  media, 
forming  both  buds  and  mycelial  threads,  hence  is  regarded  by 
some  as  a  yeast,  and  as  a  mold  by  others. 

Mycoses  due  to  Molds,  or  Hyphomycetes 

Hyphomycetes,  or  molds,  are  fungi  characterized  by  growing 
in  long  threads  or  filaments  (hyphce),  which  form  a  felt-like  mass 
(mycelium).  The  hyphae  develop  from  single  cells,  often  become 
branched,  and  finally  at  the  tip  of  the  terminal  hypha?  sporangia 
develop,  which  contain  endospores.  Some  molds,  however,  form 
chains  of  budding  exospores. 

Favus,  or  Tinea  favosa  is  a  dermatomycosis  due  to  a  mold — 
Achorion  shoerileinii — which  forms  a  yellowish  moss-like  growth 
on  culture  media.  Favus  is  characterized  by  the  formation  of 
yellowish,  concave,  scaly  crusts  composed  of  the  mold  and  des- 
quamated epithelium.  The  hair  follicles  in  the  diseased  areas  are 
usually  penetrated  by  the  mold. 

Ring*worm,  or  Tinea  trichophytina,  is  a  mycotic  inflammation 
of  the  skin,  tending  to  spread  in  a  centrifugal  manner,  and  char- 
acterized by  the  formation  of  grayish,  crusty  rings  of  infiltrated 
inflammatory  tissue,  the  center  of  which  tends  to  heal  while  the 
peripheral  part  advances.  The  hair  follicles  are  invaded  by  the 
organism,  causing  looseness  and  brittleness  of  the  hairs. 

This  dermatomycosis  is  due  to  the  Trichophyton,  of  which  there 
are  two  chief  varieties,  the  microsporon  with  spores  2[x  to  3/i  in 


184 


GENERAL   PATHOLOGY 


diameter,  found  most  frequently  in  ringworm  of  the  scalp,  and 
megalosporon  with  spores  three  times  as  large,  found  most  fre- 
quently in  ringworm  of  the  body.  The  organisms  are  best  ob- 
served by  extracting  a  diseased  hair  in  and  about  the  root  of 
which  parallel  rows  of  spores  may  be  seen  enclosed  in  delicate 
threads  of  byphae.    (Fig.  69.) 

Tinea  tonsorans  affects  the  scalp,  and  occurs  most  frequently  in 
children.  Tinea  circinata  affects  the  body,  particularly  the  moist 
folds  of  the  skin.  Tinea  sycosis,  or  "barber's  itch"  is  a  follicular 
inflammation  of  the  hairs  of  the  beard,  attended  with  active  in- 
flammation and  often  abscesses  of  the  sebaceous  glands.     Tinea 


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I  ♦  *     •  ■  SJ- 

I*    ,      VJi-.^ 1 

Fig.  69. — Invasion  of  a  human  hair  by  trichophyton:  A,  Points  at  which  the  parasitic 
fungi  coming  from  the  epidermis  are  elevating  the  cuticle  of  the  hair  and  entering  into 
its  substance.     Magnified  200  diameters.     (Sabouraud.) 

versicolor,  or  pityriasis,  due  to  the  fungus,  microsporon  furfur, 
consists  of  yellowish  brown  patches  of  desquamated  epithelium 
in  the  upper  layers  of  the  skin,  without  active  inflammation  or  in- 
volvement of  the  hair  follicles. 

Sporotrichosis  is  a  subacute  mycotic  inflammation  of  the  skin, 
and  sometimes  of  the  mucous  membrane,  characterized  by  the 
formation  of  nodules  resembling  gummata  (syphiloid  type)  or 
cutaneous  tuberculosis  (tuberculoid  type)  and  often  by  multiple 
abscesses.  When  the  mycosis  becomes  generalized,  affecting 
deeper  tissues  or  internal  organs,  it  is  apt  to  be  fatal.  The 
causal  agent  is  a  Sporothrix,  which  in  lesions  has  the  appearance 


PATHOLOGY    OF    [NFECTIOUS    DISEASES  185 

of   oval    yeast-like   bodies,    but    in    cultures    forms    long   mycelial 
tli  reads. 

Other  molds,  belonging  to  the  genera,  Aspergillus,  Mucor,  Peni- 
cillium,  etc.,  have  occasionally  been  observed  in  pathologic  condi- 
I  ions,  both  local  and  general.  The  diagnosis  of  these  mycoses,  as 
in  all  east's  of  infection  with  the  higher  bacteria,  yeasts  and  molds, 
pests  upon  the  identification  and  demonstration  of  the  organisms 
in  the  1  issues. 

THE  PROTOZOAN  INFECTIONS 

Protozoa  are  unicellular  animal  organisms,  ranging  from  3 
Hiiera  to  several  centimeters  in  length.  They  contain  one  or 
more  nuclei,  and  the  cytoplasm  presents  an  outer  portion  (ecto- 
plasm) concerned  in  prehension  of  food,  excretion  and  locomo- 
tion, and  a  central  portion  (endoplasm),  which  is  more  granular 
and  contains  the  digestive  vacuoles  and  the  nuclei.  The  major- 
ity of  pathogenic  protozoa  have  now  been  successfully  cultivated. 

Protozoa  are  divided  into  the  following  classes : 

I.  Rhizopoda  (Sarcodina),  which  have  changeable  protoplasmic 
processes  (pseudopodia).  To  this  class  belong  the  genera  Ameba 
and  Entamcba. 

II.  Mastigophcra,  which  have  flagella.  The  principal  order  is 
the  Flagellata,  to  which  belongs  the  genus  Trypanosoma. 

III.  Sporozoa,  which  have  no  flagella  or  cilia  and  which  repro- 
duce by  sporulation.  Here  are  found  the  genera  Plasmodium, 
Piroplasma  and  Coccidium. 

TV.  Infusoria,  which  have  cilia.  The  principal  subdivision  is 
the  Ciliata,  to  which  belongs  the  genus  BaJantidium. 

Amebic  Dysentery 

Amebic  dysentery  is  an  infectious  inflammation  of  the  mucosa 
and  sub  mucosa  of  the  large  intestine,  due  to  the  Entameoa  his- 
tolytica, which  measures  15  to  50//,  and  is  round  when  at  rest;  its 
pseudopods  are  short  and  blunt,  and  its  ectoplasm  and  endoplasm 
are  well  differentiated,  thus  differing  from  the  Ameba  coli  (En- 
tameba  coli),  found  in  normal  human  intestines  and  regarded  as 
harmless  parasites;  these  are  smaller  and  their  ectoplasm  and 
endoplasm  are  but  slightly  differentiated. 

The  pathogenic  amebre  are  said  to  pass  between  the  epithelial 
cells,  enter  the  submucosa,  causing  inflammatory  infiltration  and 


186  GENERAL    PATHOLOGY 

fibrinous  exudation,  leading  to  ulceration.  The  whole  colon  or 
only  localized  areas  may  he  affected.  The  ulcers  vary  in  size  from 
2  mm.  to  2  cm.,  and  have  undermined  edges,  and  yellowish  red  bases. 
The  disease  generally  becomes  chronic,  and  the  submucosa  greatly 
thickened.  Stenosis  of  the  colon  may  result  from  the  healing  and 
contraction  of  the  ulcerous  areas. 

The  arnebae  may  enter  the  mesenteric  blood  vessels,  reach  the 
liver  and  cause  focal  necrosis  or  multiple  abscesses,  or  occasionally 
a  single  large  abscess. 

Amebae  are  frequently  found  in  the  mouth,  in  tartar  of  the 
teeth,  in  carious  teeth,  abscess  of  the  jaw  and  in  pyorrhea  areo- 
laris, but  their  causal  relation  to  these  conditions  has  not  been 
proved. 


Fig.   70. — Trypanosoma  gambiense.      (Todd.) 

Trypanosomiasis 

The  trypanosomes  include  certain  flagellates  swimming  free  in 
the  blood  of  man  and  animals.  The  cell  body  is  elongated  and 
averages  1.5x25/*.  It  has  a  long  flagellum  at  the  anterior  end 
and  an  undulating  membrane  projecting  from  one  side  like  a  fan. 
Reproduction  usually  takes  place  by  longitudinal  fission.  (Fig. 
70.) 

The  following  are  the  more  common  pathogenic  trypanosomes: 

T.  evansi,  causing  surra  in  horses  and  cattle — transmitted  by  flies. 

T.  bruci,  causing  nagana  in  horses  and  cattle — transmitted  by  tsetse  flies. 

T.  equiperdum,  causing  deurine  ("horse  syphilis'"') — transmitted  by  coitus. 

T.  gambiense,  causing  sleeping  sickness  of  Central  Africa — transmitted 
by  the  bite  of  the  Glossina  palpalis,  a  fly  belonging  to  the  same  genus  as  the 
tsetse  fly,  which  causes  nagana. 


PATHOLOGY   OF    [NPECTIOUS    DISEAS  187 

The  T.  gambiense  measures  1  to  -     17  to  25fi  including  the  fla- 

gellum.     Tlu>  membrane  usually  crosses  the  body  and  motion  is 
very  active  due  to  the  screw-like  rotation  produced. 

Human  trypanosomiasis  occurs  in  two  stages;  in  the  first  the 
organisms  occur  in  small  numbers  in  the  blood,  but  may  be  absent 
for  days  at  a  time.  There  is  slight  fever  and  glandular  enlarge- 
ment. After  several  months  or  even  several  years,  the  second 
stage  begins  in  which  the  patient  becomes  apathetic  and  drowsy, 
emaciation  progresses  and  finally  complete  coma  sets  in,  followed 
by  death  in  six  or  eight  months  from  the  beginning  of  the  second 
stage.  The  organisms  are  found  in  the  blood  and  cerebrospinal 
fluid  in  This  stage.  The  spinal  fluid  is  cloudy,  and  the  postmortem 
findings  show  a  meningo-encephalomyelitis  and  enlargement  of  the 
spleen,  liver  and  lymphatic  glands. 

Leishmaniases 

The  Leishmaniases  include  two  tropical  visceral  and  one  cuta- 
neous disease.  Kala-azar,  or  dumdum  fever  (India  and  Africa)  is 
due  to  the  Leishmania  donovani,  organisms  belonging  to  the  flagel- 
lates and  related  to  the  trypanosomes.  The  disease  is  characterized 
by  splenomegaly,  enlarged  and  cirrhotic  liver,  both  organs  being 
filled  with  the  parasites,  progressive  anemia  and  remittent  fever, 
running  a  course  of  six  to  nine  months,  with  a  mortality  of  96  per 
cent. 

Infantile  kala-azar  or  Splenomegaly  is  probably  identical  with 
the  above  type,  occurring  in  the  Mediterranean  countries. 

Oriental  sore  or  delhi  boil  is  due  to  Leishmania  tropica  and 
characterized  by  ulcerating  nodules  on  the  face  and  elsewhere. 

Malaria 

Malaria  is  a  protozoan  disease,  characterized  by  paroxysms  of 
chills,  fever  and  sweating,  and  anemia  due  to  destruction  of  the 
red  blood  cells.  It  is  due  to  the  Plasmodium  or  Hematozoon  ma- 
lariae  (Laveran). 

This  protozoon  has  two  life  cycles — one  in  man  (the  intermedi- 
ate host)  and  one  in  the  Anopheles  genus  of  mosquito  (the  true 
or  definite  host).  "When  man  is  bitten  by  an  infected  mosquito, 
spores  (or  merozoites)    of  the  Plasmodium  enter  his  red  blood 


188  GENERAL   PATHOLOGY 

cells,  grow  upon  its  substance  and  dissolve  its  hemoglobin,  until 
the  parasite  becomes  as  large  or  larger  than  the  cell,  swelling 
the  latter  until  only  a  faint  ring  remains.  Then  division  (seg- 
mentation or  sporulation)  takes  place,  occurring  more  or  less 
simultaneously  in  all  the  organisms,  thus  accounting  for  the  par- 
oxysms of  the  disease.  Segmentation  destroys  the  red  cell,  and 
the  young  protozoa  escape  into  the  blood  plasma  and  each  enters 
a  new  red  cell  to  produce  a  second  generation.  AVhile  most  of 
the  organisms  divide  as  just  described  there  are  some  which 
grow  to  full  size,  destroy  the  red  cell,  but  do  not  segmentate. 
These  "extracellular  bodies"  are  finally  eliminated,  unless  a  ma- 
larial patient  be  bitten  by  the  mosquito  and  some  of  these  bodies 
be  sucked  up  with  the  blood.  In  the  stomach  of  the  mosquito, 
these  bodies,  which  are  sexually  differentiated  (gametocytes) 
find  conditions  favorable  for  sexual  development ;  Avhen  the  fe- 
male cell  becomes  fertilized,  it  penetrates  the  stomach  wall  and 
becomes  encysted,  and  when  the  cyst  ruptures  the  sporozoites 
migrate  throughout  the  body  of  the  mosquito,  accumulating  par- 
ticularly in  the  poison  gland  (a  modified  salivary  gland)  and 
are  thus  in  position  to  be  inoculated  into  man. 

Stagnant  pools,  swamps,  etc.,  are  not  the  habitat  of  the  Plas- 
modium, but  merely  the  breeding  places  of  the  mosquito.  It  is  the 
female  of  about  seven  or  eight  species  of  the  Anopheles  genus  by 
which  infection  occurs. 

The  following  features  serve  to  distinguish  the  Anopheles  from 
the  common  mosquito  (Culex) : 

The  Anopheles  The  Culex 


The  palpae  of  both  sexes  nearly  The   female   palpae   very   short, 

equal  to  proboscis.  the  male  palpae  very  long. 

In     resting     on     perpendicular  The  body  is  parallel  to  the  wall. 

wall,  the  body  is  inclined  at 

angle. 

The  wings  are  spotted  usually.  Wings  never  spotted. 

The    head,    thorax,    and    body  Lower  part  of  body  is  joined  to 

form  a  straight  line.  thorax  at  an  angle. 

The   larvae   are   parallel   to  the  The  larvae  hang  downward  from 

surface  of  the  water.  the  surface  of  the  water. 


PATHOLOGY   OF    INFECTIOUS   DISEASES  189 

The  Plasmodia  are  of  three  varieties: 

(1)  P.  vivax,  causing"  tertian  fever,  segmentates  every  48 
hours,  i.  e.,  on  the  third  day,  into  12  to  24  merozoites.  When 
young  the  organisms  are  hyaline  and  actively  motile  (ameboid), 
bid  as  time  for  segmentation  approaches  they  become  granular 
and  nonmotile.  The  fully  grown  parasite  and  the  gametocytes 
are  larger  than  the  average  red  blood  cell. 

(2)  P.  malaria',  causing  quartan  fever,  segmentates  in  72  hours, 
into  6  to  14  merozoites  (usually  eight.)  The  young  parasites  are 
not  actively  motile.  The  fully  grown  forms  and  the  gametocytes 
are  about  as  large  as  the  red  blood  cell. 

(3)  P.  falciparum,  causing  aestive-autumnal  fever,  a  pernicious 
and  often  fatal  type,  occurs  in  two  forms:  (a)  the  quotidian  which 
segmentates  every  day  within  the  bone  marrow  and  internal  or- 
gans, into  6  to  16  merozoites.  The  young  are  actively  motile. 
The  fully  grown  forms  and  the  gametocytes  (which  are  crescen- 
tic,  "half-moon"  forms)  are  smaller  than  the  red  cell,  (b)  The 
tertian  form  segmentates  in  48  hours.  This  would  cause  the  oc- 
currence of  irregular  paroxysms,  but  distinct  paroxysms  are  sel- 
dom seen  in  this  form  of  malaria. 

Gametocytes  with  flagella  may  be  seen  in  all  types. 

The  paroxysmal  chills,  fever  and  sweating  are  believed  to  be 
due  to  toxins  liberated  during  segmentation.  When  two  groups 
of  P.  vivax  segmentate  on  alternate  days,  daily  paroxysms,  or 
"quotidian  fever,"  results. 

Pathologically,  destruction  of  the  red  cells,  with  melanemia, 
relative  and  absolute  leucopenia,  and  liberation  and  alteration 
of  the  hemoglobin  are  the  principal  features.  Hemoglobinuria 
occurs,  and  the  internal  organs,  as  liver,  spleen,  bone-marrow  and 
brain  are  darkly  pigmented.  The  spleen  is  enlarged  in  all  cases, 
soft  and  friable  in  acute  cases,  and  filled  with  infected  red 
blood  cells ;  focal  areas  of  necrosis  are  seen.  In  chronic  cases 
the  spleen  may  become  enormous  and  sclerotic,  with  much  of 
the  pulp  and  follicles  destroyed  ("ague  cake.") 

Texas  cattle  fever  ("bovine  malaria")  characterized  by  acute 
fever  and  destruction  of  red  blood  cells,  is  due  to  the  Piroplasma 
bigeminum,  belonging  to  the  Sporozoon  class  of  parasites,  which 
is  transmitted  by  the  cattle  tick. 


190  GENERAL   PATHOLOGY 

Coccidiosis 

Coccidiosis,  primarily  a  disease  of  rabbits  and  occasionally 
transmitted  to  man.  is  due  to  the  Coccidium  oviforme,  an  ovoid 
granular  body,  enclosed  in  a  tough  capsule,  and  measuring  15  to  20 
by  20  to  40  miera.  It  occurs  in  the  tissues,  a  daily  of  the  liver, 
where  it  forms  cyst-like  nodules,  containing  degenerated  host  cells 
in  which  the  parasites  are  embedded.  They  are  found  also  in  the 
intestinal  epithelium,  and  sporulate  after  elimination  from  the 
body  in  the  stools.  Infection  may  occur  by  ingestion  of  the  spores. 
The  liver  besides  containing  the  specific  nodules  becomes  cirrhotic. 
Other  organs  are  rarely  involved. 

The  Balantidium  coli,  an  infusorial  parasite,  has  been  found  in 
the  intestines  of  swine  and  occasionally  of  man,  and  various  patho- 
logic conditions,  particularly  colonic  diarrhea,  have  been  attrib- 
uted to  it.  It  is  found  in  the  stools  and  blood,  is  ovoidal  in  form 
(0.06  to  0.1  mm.)  and  covered  with  numerous  cilia. 

INFECTIOUS  DISEASES  CAUSED  BY  UNDETERMINED 
MICROORGANISMS 

Measles 

^Measles  (Rubeola-  is  an  acute,  contagious  disease,  due  to  a 
filterable  virus,  i.e..  a  microorganism  small  enough  to  pass 
through  the  pores  of  a  porcelain  filter,  the  filtrate  causing  the 
disease  when  susceptible  animals  are  inoculated. 

Pathologically  there  is  mild  pharyngitis,  rhinitis  and  conjunc- 
tivitis with  a  mottled  eruption  of  the  skin,  consisting  of  brick- 
red,  slightly  elevated,  papules,  which  run  together  to  form  eres- 
eentic  patches.  The  skin  is  hypereinic  and  slightly  swollen,  par- 
ticularly upon  the  face.  The  eruption  is  followed  by  a  powdery 
desquamation.  Both  the  eruptive  lesions  and  the  desquamated 
scales  contain  the  virus,  and  may  convey  the  disease,  this  being 
true  also  of  other  exanthemata,  or  diseases  attended  with  char- 
acteristic skin  eruptions. 

In  severe  cases  of  measles  bronchopneumonia  and  nephritis  may 
develop.  In  the  severe  and  usually  fatal  form — the  black  mea- 
sles— the  toxemia  is  great,  and  the  eruption  becomes  hemorrhagic 
and  dark. 


PATHOLOGY    OF    INFECTIOUS    DISEASES  191 

German  Measles 

German  measles,  or  rubella,  is  a  mild  contagious  disease,  char- 
acterized  by  red  punctate  spots  in  the  pharynx,  followed  by  more 
or  less  circumscribed  spots  on  the  reddened  skin,  which  do  not 
fuse  to  form  mottled  patches,  as  in  measles.  Swelling  of  the 
postcervical  glands  is  seen,  and  rarely  there  may  be  distinct 
pharyngitis,  bronchitis,  etc. 

Chicken  Pox  or  Varicella 

( Ihicken  pox,  or  varicella,  is  a  mild  contagious  disease  char- 
acterized by  a  red  papular  eruption  which  becomes  vesicular. 
The  papules  are  usually  discrete  and  few  in  number,  although 
occasionally  they  are  numerous  and  may  become  very  large,  re- 
sembling pemphigus. 

Scarlet  Fever  or  Scarlatina 

Scarlet  fever,  or  scarlatina,  is  an  acute  contagious  disease  char- 
acterized by  inflammation  of  the  mucous  membrane  of  the  nose, 
mouth,  throat  and  eyes,  as  in  measles,  but  usually  of  greater  in- 
tensity. The  lingual  papillae  swell  and  redden  ("strawberry 
tongue"),  and  the  throat  is  spotted  with  fine  red  points.  The 
rash,  first  appearing  upon  the  body  and  spreading  to  the  ex- 
tremities, consists  of  small  red  spots  which  fuse  as  the  skin 
swells,  thus  forming  an  intensely  red,  uniform  erythema. 

Endocarditis,  pericarditis  and  nephritis,  as  well  as  broncho- 
pneumonia are  more  frequent  than  in  measles,  and  the  glands  of 
the  neck  often  suppurate.  In  fatal  cases  focal  necrosis  is  usually 
seen  in  the  internal  organs. 

Mumps,  or  Acute  Epidemic  Parotitis 

Mumps,  or  acute  epidemic  parotitis  is  an  acute  contagious  in- 
flammation of  the  parotid,  less  often  of  the  submaxillary  salivary 
glands.  Usually  the  glands  on  both  sides  are  affected,  resulting 
in  extensive  and  painful  swelling,  due  to  a  serous  exudation.  The 
salivary  ducts  and  the  contiguous  lyinph  glands  are  also  usually 
inflamed,  and  metastatic  orchitis  and  epididymitis  are  not  in- 
frequent, especially  in  adults. 


192  GENERAL   PATHOLOGY 

Measles,  rubella,  varicella,  scarlatina  and  mumps  are  distinctly 
the  diseases  of  childhood  or  youth.  Their  pronounced  contagious 
character  results  in  early  infection,  and  the  usual  life-long  immu- 
nity conferred  makes  second  infections  or  recurrences  and  in- 
fections in  adults  very  infrequent. 

Acute  Poliomyelitis,  or  Infantile  Paralysis 

Acute  poliomyelitis,  or  infantile  paralysis,  is  a  disease  of  child- 
hood when  occurring  sporadically,  but  in  epidemic  form  appar- 
ently affects  any  age,  though  still  more  frequent  among  the 
young.  It  is  an  acute  general  infection  characterized  by  diffuse 
cerebrospinal  lesions,  especially  inflammation  of  the  anterior 
horns  of  the  spinal  gray  matter,  with  paralysis  and  wasting  of 
the  muscles,  degenerative  changes  in  the  nerves,  hyperplasia  of 
lymphoid  structures  and  degenerative  changes  in  the  liver,  lungs, 
kidneys,  and  other  organs. 

The  pia  mater  and  arachnoid  are  inflamed,  accompanied  by 
marked  round-cell  infiltration;  groups  of  ganglion  cells  become  in- 
flamed, degenerate  and  disappear  and  their  nerve  fibers  neces- 
sarily degenerate.  The  whole  cord  becomes  edematous.  In  se- 
vere and  fatal  cases  the  medulla,  pons,  cerebellum  or  cerebrum 
are  similarly  affected. 

The  virus  is  filterable  and  is  present  in  the  brain,  cord,  spinal 
fluid,  nasopharynx,  blood  and  gastrointestinal  contents.  Inocu- 
lated into  the  brain  of  a  monkey,  the  symptoms  and  lesions  of 
the  disease  are  said  to  result.  Small  bacteria-like  bodies  have 
been  discovered,  but  their  nature  and  relation  to  this  disease 
have  not  been  fully  established.  Direct  transmission  through  the 
nasopharynx  to  the  nervous  system  is  the  most  probable  mode  of 
infection  according  to  Flexner,  while  Rosenau  reported  the  trans- 
mission from  monkey  to  monkey  by  the  bite  of  the  common 
stable  fly.     One  attack  of  poliomyelitis  confers  immunity. 

Acute  Articular  Rheumatism 

Acute  articular  rheumatism  is  probably  an  infectious  disease 
and  apparently  due  to  a  streptococcus,  but  this  has  not  yet  been 
definitely  established.  The  lesions  consist  of  an  arthritis,  the  in- 
flammation involving  all  the  structures  of  the  joint,  and  often 
the  periarticular  structures.     The  joints  are  usually  involved  in 


PATHOLOGY   OF   INFECTIOUS   DISEASES  193 

succession  (polyarthritis).  The  knee  is  the  mosl  frequently  af- 
fected, then  the  ankles,  elbows,  and  wrists.  Endocarditis,  peri- 
carditis or  myocarditis  are  frequenl  complications.  Sudamina 
are  common,  accompanying  the  profuse  sweating,  and  subcuta- 
neous nodes  (or  aggregations  of  round  or  spindle  cells)  as  large  as 
buck  shot  may  sometimes  be  felt  on  the  fingers,  wrists,  elbows 
and  elsewhere. 

Dengue 

Dengue  is  an  acute  contagious  disease  of  tropical  origin,  which 
lias  invaded  Europe,  the  United  States,  and  South  America.  A 
mosquito  is  believed  to  be  the  eontagium  carrier,  but  fomites  may 
also  transmit  the  disease.  There  is  a  polymorphous  eruption  on 
the  body,  face,  and  arms,  which  may  be  scarlatiniform,  urticarial, 
vesicular  or  even  pustular.  Many  of  the  joints  become  swollen 
one  after  another  and  painful  ("break-bone  fever"  and  "dandy 
fever" — terms  given  in  allusion  to  the  peculiar  gait  necessarily 
assumed).  The  muscles  become  painful  and  swollen.  Prostra- 
tion, convulsions  and  coma  occur  in  fatal  cases.  One  attack  does 
not  confer  immunity,  three  or  four  recurrences  being  reported. 

Yellow  Fever,  or  Typhus  Icteroides 

Yellow  fever,  or  typhus  icteroides  is  an  acute  infectious  dis- 
ease, endemic  in  American  tropics  and  contracted  through  the 
bite  of  a  mosquito — Stegomijia  calopus.  The  mosquito  serves  as 
a  host  for  one  of  the  life  cycles  of  the  microorganism,  for  an  in- 
fected mosquito  (one  observed  to  draw  blood  from  a  yellow  fever 
patient)  can  not  infect  a  healthy  person  until  after  the  lapse  of  at 
least  12  days.  The  unknown  organism  is  in  the  peripheral  blood 
only  in  the  first  three  days  of  the  disease,  because  a  mosquito  can 
convey  the  infection  only  when  it  bites  the  patient  during  that 
time;  likewise  only  blood  taken  during  that  time  will  successfully 
inoculate  a  healthy  person.  The  virus  is  filterable.  One  attack 
confers  immunity. 

Pathologically  there  is  fatty  degeneration  of  the  liver  and  acute 
hemorrhagic  inflammation  of  the  kidneys  with  degenerative  changes 
in  the  parenchyma.  Hemorrhages  occur  into  the  mucous  and  se- 
rous membranes :  Icterus,  albuminuria,  hematemesis  and  fever 
with  great  prostration  are  the  chief  features. 


194  GENERAL   PATHOLOGY 

Typhus  Fever 

Typhus  fever,  or  ship  or  famiue  fever  is  an  acute  contagious 
disease  attended  with  a  macular  skin  eruption  (roseola?)  later 
changing  to  copper-colored  petechia?,  catarrhal  inflammation  of 
the  air  passages,  intense  toxemia  with  high  temperature  and  severe 
nervous  symptoms — the  latter  simulating  those  of  typhoid  fever. 
The  spleen  is  enlarged,  soft  and  easily  ruptured.  The  liver  is 
swollen,  soft  and  grayish.  In  severe  cases  gastrointestinal 
hemorrhages,  ulcerations  of  the  esophagus  and  acute  myocardi- 
tis are  observed.  In  fatal  cases  the  blood  is  dark  and  fluid  and 
rapidly  putrefies.  The  virus  is  believed  to  be  transmitted  by  the 
body  louse,  Pediculus  vestimenti,  or  "cootie." 

Smallpox,  or  Variola 

Smallpox,  or  variola,  is  an  acute  contagious  disease  marked  by 
an  eruption  upon  the  skin  of  hard,  shot-like  papules,  which 
change  in  a  feAv  days  to  vesicles,  and  finally  to  pustules.  These 
pocks  may  remain  discrete  or  become  confluent.  Finally  the 
exudate  of  the  pustule  dries  and  a  necrotic  crust  forms.  When 
the  lesions  are  confined  to  the  epidermis  no  deformity  or  "pit- 
ting" results,  but  if  the  corium  is  much  involved  cicatricial 
scars  are  formed.  Other  changes  that  may  occur  are  diffuse 
suppurative  inflammation  of  the  skin,  ulcerations  of  the  mucous 
membranes,  ulceration  of  the  lymph  glands,  degenerative  changes 
of  the  liver,  kidneys,  and  spleen.  In  the  virulent  form,  Variola 
purpura,  or  "black  smallpox,"  hemorrhage  into  the  lesions  or 
pocks  occurs,  giving  them  a  purple  or  dark  color,  often  inky  black. 
In  this  form  death  may  ensue  before  the  pustular  or  even  the  vesic- 
ular stages  are  reached. 

Infection  is  direct  by  means  of  the  eruptive  lesions,  especially 
the  dried  pustular  exudates,  but  the  blood,  secretions  and  excre- 
tions may  all  convey  the  virus.  One  attack  usually  confers  life- 
long immunity,  and  vaccination  with  the  virus  of  cowpox  gives 
immunity  for  variable  periods  ranging  from  one  year  to  many 
years. 

Foot-and-mouth  Disease 

Foot-and-mouth  disease,  or  epidemic  stomatitis,  is  a  contagious 
disease  of  cattle  communicable  to  man,  occurring  in  Europe  and 


PATHOLOGY    OF    [NFECTIOUS   DISEASES  195 

America.     There   is   swelling   of   the   mucous  membrane   of  the 

mouth  with  formation  of  small  clear  vesicles,  and  similar  lesions 
on  the  udders  and  hoofs.  In  man  the  mouth  and  hands  are 
usually  affected.  The  virus  is  filterable.  One  attack  gives  im- 
munity. Infection  follows  the  use  of  milk  or  contact  with  af- 
fected animals. 

Kocky  Mountain  Fever 

Eocky  mountain  fever  is  an  acute  contagious  disease  observed 
in  Montana,  Idaho,  Wyoming,  and  Nevada.  It  is  characterized 
by  epistaxis,  fever  lasting  one  to  two  weeks,  bronchitis,  nephri- 
tis, hepatic  and  splenic  enlargement,  slight  jaundice,  moderate 
leucocytosis,  muscular  pains  and  a  macular  rash  over  the  body 
which  does  not  disappear  upon  pressure  (except  at  the  begin- 
ning.) The  virus  is  transmitted  by  a  tick,  Dermacentor  reticula- 
tus  or  occidentalis,  and  is  contained  in  the  blood,  but  is  not  filter- 
able. 

METAZOA 

Among  the  Metazoa  (multicellular  animal  organisms)  the  fol- 
lowing parasites  are  of  interest  to  the  pathologist. 

1.  Helminthes,  Vermes  or  Worms. — These  are  endoparasites, 
infestation  with  which  is  called  Helminthiasis.  They  may  be 
divided  into : 

(A)    Platyhelminthes,    (Flat worms) — flat,    bilaterally    symmetrical,    requiring 
two  hosts  for  complete  life  cycle. 
Subdivided  into: 

(a)  Trematodes    or   Flukes — oval,    leaf-like,    unsegmented,    having 

incomplete  alimentary  canal;  majority  hermaphroditic. 

(b)  Cestodes   or   Tapeworms — tape-like,   segmented,   no   alimentary 

canal;   all  hermaphrodites. 
The  Flukes  include : 

(1)  Distomum  hepaticum,  or  Liver  Fluke. 

(2)  "  buski,    or   Intestinal   Fluke. 

(3)  "  pulmonale,  or  Lung  Fluke. 

(4)  Schistosomum  hematobium  or  Blood   Fluke. 
The  Tapeworms  include: 

(1)  Tenia  solium,  or  Pork  Tapeworm. 

(2)  "       saginata,  or  Beef  Tapeworm. 

(3)  Dibothriocephalus  latus,  Fish  Tapeworm. 

(4)  Tenia  echinococcus,  or  Dog  Tapeworm. 

(5)  "       nana,  or  Dwarf  Tapeworm. 

(6)  "       canina,  or  Dog  and  Cat  Tapeworm. 


196  GENERAL   PATHOLOGY 

(.15)  Nematodes  or  Bound  Worms — elongated,  cylindrical,  tapering  toward 
ends,  bisexual  in  nearly  all  cases,  the  female  1  icing  twice  as  large  as 
the  male.     These  include: 

(1)  Ascaris  lumbricoides — Common  round  worm. 

(2)  Oxyuris  vermicularis — Thread  or  seat-worm. 

(3)  Trichocephalus  dispar — Whipworm. 

(4)  Strongyloides  Intestinalis  (Anguillula). 

(5)  Ankylostoma  duodenale  or  Hookworm. 

Uncinaria  ameiicana — American  Hookworm. 

(6)  Trichina  spiralis. 

(7)  Filaria  medinensis — Guinea-worm. 

(8)  "  sanguinis  hominis   (F.  bancrofti). 

(9)  Eustrongylus  gigas. 

II.  Arthropoda  (having  "jointed  feet").  These  are  epipara- 
sites,  which  cause  various  forms  of  dermatitis.  Some  are  dis- 
ease carriers. 

(A)  Arachnida — "spider-like"  forms,  air-breathing: 

(a)   Acari — including  mites  and  ticks. 

(i  )   Mites   (1)   Leptus  autumnalis — Harvest  mite. 

(2)   Acarus    scabiei — Itch  mite, 
(ii)    Ticks   (I)   Dermacenter   reticulatus — believed   to   be   car- 
rier in  Rocky  Mountain  Fever. 
(2)   Margarbpus    annulatus — believed    to    be    car- 
rier in  Texas  cattle  fever. 

(B)  Insecta — having  "cut  into"  or  segmented  bodies. 

(1)  Pediculus  capitis  or  Head  louse. 

(2)  "         pubis  or  Crab  louse. 

(3)  "         vestimenti  or  Body  louse,  "cootie." 

(4)  Cimex  lectularius  or  Bed  bug. 

(5)  Pulex    irritans    or    common    Flea. 

(6)  "        penetrans  or  Jigger,  Chigger,  or  Chigoe. 

(7)  "        cheopis    or   Rat   flea   of    India,   Australia   and   the   Phil- 

lipincs,  believed  to  convey  B.  pestis  which  causes  bubonic 
plague. 

Trematod.es. — The  ova  are  deposited  in  water  and  developed 
into  ciliated  embryos  (miracidia),  which  enter  a  small  snail  (mol- 
lusk)  in  which  they  develop  into  motile  bodies  (cercarise).  These 
leave  the  mollusk  (intermediate  host),  and  swim  about  in  the 
water,  whence  they  may  enter  man  (definitive  host). 

Of  the  many  fluke-worms  the  following  only  are  important: 
Distomum  hepaticum,  or  Liver  fluke,  is  oval  (8x25  mm.)  hav- 
ing two  suckers  ("distomum")   and  a  median  genital  pore  con- 
taining male  and  female  organs   (hermaphrodite).     The  mature 
fluke-worm,  yellowish  brown  or  pink  in  color,  is  found  in  the 


I'\T1H>I,()<;y    OF    [NFECTIOUS    DISEASES 


L97 


bile  duds  of  lierbivora,  rarely  in  man,  and  if  in  sufficienl  num- 
bers, will  canst'  obstructive  inflammation  of  the  ducts.  In  sheep 
tlic  liver  is  often  greatly  degenerated  ("liver  rot.")  (Fig.  71.) 

Distomum  buski  is  the  largest  fluke-worm  found  in  the  human 
intestine  (25-70  5-14  nun.);  occurs  chiefly  in  Eastern  and  South 
ern  Asia. 

Distomum    pulmonale    (Paragonimus    westermani)    or    Lung 
Fluke. — This   is   about    one-third   as   large    as    I),    hepatica,   and 

/V-W^*    ,/t    .Vet. 

SERF 

"-■-MM.  'A  -«• 


Fig. 


'1. — The    common    liver-fluke    (Fasciola    hepatica),    enlarged    to    show    the    anatomic 
characters.      (Afn-r    Stiles.) 


found  in  cyst-like  cavities  in  the  lungs.    It  is  apt  to  cause  hemop- 
tysis (parasitic  hemoptysis  of  Eastern  Asia). 

Schistosomum  hematobium,  or  Blood  Fluke. — This  worm  is  bi- 
sexual, the  male  measures  12x0.5  mm.,  and  is  white  in  color,  the 
female,  20x0.25  mm.,  is  white  anteriorly  and  gray  posteriorly. 
The  female  is  attached  to  the  male,  lying  in  a  groove  on  the  ven- 


198  GENERAL   PATHOLOGY 

tral  surface  of  the  latter.  They  occur  in  the  veins  of  the  bladder 
and  rectum  (very  rarely  entering  the  general  circulation),  and 
cause  local  inflammation,  ulceration  and  hematuria  (Bilhar- 
ziasis  of  Africa  and  Asia).  The  ova,  yellow,  translucent  and  oval 
(1  mm.),  may  often  be  found  in  the  urine  or  feces. 

The  Cestodes,  or  Tapeworms 

Tenia  Solium,  or  Pork  Tapeworm. — This  parasite  is  2  to  4  me- 
ters long,  occasionally  much  longer,  and  consists  of  a  small  head 
(1  mm.),  spherical  and  dark  brown  in  color,  (scolex),  with  four 
disc-like  suckers  and  a  rostellum  armed  with  a  double  row  of 
hooklets  (about  30)  on  its  anterior  end.  The  neck  is  thread- 
like and  one  inch  long.    The  body  (strobila)  is  composed  of  600 


Fig.    72. — Head    of    T:enia    solium.      (Mosler    and    Peiper.) 

to  900  segments  (proglottides)  which  increase  in  size  from  the 
neck  backward,  becoming  smaller  again  near  the  posterior  end. 
The  largest  segments  measure  about  6x10  mm.  Each  segment 
(proglottis)  is  hermaphroditic  and  has  a  uterus  with  seven  to  fif- 
teen branches.  Groups  of  segments  may  be  discharged  from  the 
bowel  at  intervals,  and  each  segment  has  independent  motility. 
The  ova  develop  in  utero  into  embryos  having  six  hooklets,  and 
surrounded  with  a  striated  shell  (onchosphere).  When  ingested  by 
the  hog,  or  rarely  other  animals,  even  man,  the  shells  are  dissolved 
in  the  stomach  and  the  embryos  pass  into  the  tissues  where  they 
form  cysts  (cysticerci)  and  develop  a  scolex.  The  cysts  are  visible 
to  the  naked  eye,  and  constitute  the  "measled"  pork  or  other 
meat.    When  insufficiently  cooked  pork  is  eaten,  the  scolex  or  head 


l'ATIKtl.OGY   OF   INFECTIOUS    DISEASES  199 

attaches  itself  to  the  mucosa  of  the  upper  ileum  and  a  tapeworm 
develops,  reaching  its  full  growth  in  about  four  months.  (Fig. 
72. 

Tenia  Saginata  or  Beef  Tapeworm. — This  is  twice  as  long  and 
lias  a  head  twice  as  large  as  the  T.  solium.  The  head  has  four 
suckers,  but  no  rostellum  or  hooklets.  The  segments  usually 
number  over  1000,  the  largest  measuring  7x20  mm.  The  uterus 
has  20  to  35  branches,  and  the  ova  are  larger  and  more  oval  than 
those  of  T.  solium;  the  segments  also  are  more  motile.  The  lar- 
va? are  found  in  the  muscles,  liver,  and  lungs  of  the  ox. 

Dibothriocephalus  Latus  or  Fish  Tapeworm. — This  is  the  larg- 
est parasite  of  man.  It  is  common  in  Asia  and  Europe,  is  gray- 
ish yellow  in  color,  measures  5  to  9  meters  in  length  and  has 
3000  to  4000  segments,  short  and  broad  in  the  middle  but  di- 
minishing toward  either  end.  The  head  is  very  small,  flattened, 
elongated  and  has  a  deep,  longitudinal  groove  on  each  side.  The 
ova  have  brown,  operculated  shells,  and  develop  in  the  water  to 
motile,  ciliated  embryos,  provided  with  six  hooklets,  which  enter 
an  intermediate  host,  usually  the  pike,  perch  or  other  fresh- 
water fish.    The  complete  life  history  of  this  worm  is  not  known. 

The  symptoms  produced  by  the  larger  intestinal  tapeworms 
are  usually  insignificant,  and  in  the  majority  of  instances  these 
worms  occasion  no  harm;  however,  when  present  in  great  num- 
bers, they  may  cause  intestinal  obstruction,  and  various  reflex 
nervous  symptoms,  and  occasionally  grave  anemic  conditions, 
believed  to  be  due  to  hemolytic  poisons  formed  by  the  death  and 
decomposition  of  portions  of  the  worm. 

Tenia  Echinococcus. — This  is  a  small  tapeworm,  2  to  6  mm. 
long,  inhabiting  the  intestines  of  dogs,  wolves,  foxes,  etc.  It  is 
composed  of  a  head  and  three  segments.  The  head  is  about  one- 
third  as  large  as  that  of  T.  solium,  but  otherwise  resembles  it  in 
structure  and  equipment.  The  last  segment  alone  is  mature,  and 
as  large  or  larger  than  the  remainder  of  the  worm.  The  uterus 
consists  of  a  central  trunk  with  lateral  branches.  The  ova  are 
thin-shelled  and  resemble  the  ova  of  the  pork  tapeworm.  When 
ingested  by  man  the  embryo  passes  to  the  liver,  lungs  and  other 
parts,  forming  a  cyst — the  hydatid  cyst. 

The  hydatid  or  echinococcus  cyst  has  a  wall  composed  of  two 
layers,  an  outer  layer  of  elastic  cuticle   (ectocyst)   and  an  inner, 


200  GENERAL   PATHOLOGY 

germinal  layer,  (endocyst).  The  entire  cyst  becomes  encapsulated 
by  fibrous  tissue  from  the  tissues  of  the  host.  From  the  inner 
germinal  layer,  bud-like  "brood  capsules"  develop  and  project 
into  the  cavity  of  the  cyst ;  from  the  brood  capsules  scolices  (heads 
with  suckers  and  booklets)  form  as  external  growths.  The  inte- 
rior of  the  cyst  is  filled  with  clear  fluid,  nonalbuminous,  but  rich  in 
sodium  chloride  and  other  salts. 

From  the  primal  or  "mother  cysts,"  secondary  cysts,  "daugh- 
ter" and  even  "granddaughter  cysts"  may  develop,  each  capable 
of  forming  brood  capsules  and  solices.  Thus  from  one  ovum, 
thousands  of  solices  may  develop.  Hydatid  cysts  vary  in  size  from 
a  walnut  to  an  apple ;  occasionally  they  grow  to  a  very  large  size, 
especially  when  secondary  cysts  arise.     When  large  they  are  apt 


Fig.   73. — T;ienia  echinococcus,   enlarged    (Mosler   and   Peiper). 

to  rupture  into  the  peritoneum,  lungs  and  other  organs  or  struc- 
tures with  fatal  results.  Small  cysts  may  become  inactive  after 
a  time,  or  die  and  be  replaced  with  fatty,  fibrous  or  calcareous  ma- 
terial.    (Fig.  73.) 

Tenia  nana,  or  dwarf  tapeworm,  is  one  inch  long,  often  less, 
occurring  in  rats  and  other  animals  and  rarely  in  man.  The  inter- 
mediate host  is  believed  to  be  an  insect. 

Tenia  canina  is  a  worm  found  in  dogs  and  cats,  sometimes  in 
man,  especially  children.  It  is  15  to  35  cm.  long;  its  head  has 
four  suckers.  The  mature  segments  are  reddish  in  color,  and  re- 
semble cucumbers  in  shape,  hence  also  called  T.  cueumcrina. 

The  Ascaris  lumbricoides  is  a  frequent  parasite  of  man,  par- 
ticularly of  children.  The  female  ascaris  measures  20  -  35  cm. 
x  4_6  mm.    These  Avorms  are  brown  or  pink  in  color,  cylindrical 


PATHOLOGY    OP    INFKCTIOUS    DISKASKS 


201 


ami  nonsegmented,  resembling  the  common  earth  worm  in  out- 
line. They  are  transversely  striated  and  have  four  longitudinal 
ridges.  The  head  is  small,  and  the  mouth  is  surrounded  with 
three  lips.  The  tail  of  the  female  is  straight,  that  of  the  male 
is  curved.  Infestation  occurs  through  ingestion  of  the  ova,  which 
develop  into  worms  in  the  upper  and  middle  portions  of  the  ileum. 
Usually  only  a   Jew   worms  are  present  at  one  time,  and  these 


Fig.    74. — Ascans    lumbricoides :      A,    female;    B,   male;    C,    egg,    magnified    300    diameters; 
b,   head,   magnified.      (After   Perls.) 

may  cause  few  or  no  symptoms,  but  sometimes  great  numbers 
occur  and  may  cause  obstructive  symptoms,  or  may  migrate  into 
the  gall  ducts,  stomach,  esophagus,  trachea  and  nose.  Fatal 
plugging  of  the  pharynx  has  occurred.  The  parasite  secretes 
irritating,  volatile  aldehydes  and  fatty  acids,  which  may  account 
for  the  anorexia  and  nervous  manifestations  that  frequently  oc- 
cur.    (Fig.  74.) 


202  GENERAL   PATITOEOGY 

Oxyuris  vermicularis,  or  Pin-worm,  Thread-worm  or  Seat- 
worm.— These  worms  are  small,  white,  round,  the  female  meas- 
uring 10  x  0.4  mm.  and  having  a  straight  posterior  end,  that  of  the 
male  being  curved.  These  parasites  are  very  common  in  children. 
Infestation  occurs  through  ingestion  of  the  ova,  and  the  worms 
mature  in  the  small  intestine.  After  impregnation  the  female 
descends  into  the  rectum  where  the  eggs  are  deposited. 

Many  of  the  ova  and  worms  are  discharged  with  the  feces, 
but  some  of  the  latter  pass  out  per  anum  by  their  own  movements, 
causing  considerable  irritation  and  nervous  irritability.  Emi- 
gration occurs  principally  at  night  and  the  parasites  are  often 
found  upon  the  bed  clothing. 

Trichocephalus  dispar  or  Whipworm.^-The  anterior  end  of  this 


Fig.    75. — Male    Trichocephalus    dispar    or    whipworm.      A    large    part    of   the    cephalic    end 
has   transfixed   a   fold    of   intestinal   mucosa.      (Cohen.) 

worm  is  thread-like,  resembling  the  lash  of  a  whip,  and  the  pos- 
terior part  is  thicker  ("handle")  and  straight  in  the  female,  but 
curled  in  the  male.  The  female  is  45  to  50  mm.  long,  the  male 
a  few  millimeters  less.  The  ova  incubate  in  water  or  mud. 
When  ingested  the  embryo  develops  and  matures  in  the  cecum, 
occasionally  entering  the  appendix.  The  worm  attaches  itself  Im- 
penetrating or  transfixing  a  fold  of  mucous  membrane  with  its 
thin  anterior  end.  It  is  a  frequently  encountered  parasite,  and 
usually  quite  harmless,  but  occasionally  serious  anemia  has  been  ob- 
served.    (Fig.  75.) 

Strongyloides     intestinalis     (Aguillula     intestinales).— These 
small  (2x0.30  mm.)  worms  occur  in  the  upper  intestinal  tract  in 


ATHOLOGT?    OF    INFECTIOUS    DISEASES 


203 


association   with   certain   forms  of  diarrhea   in   the   tropics,  bu1 
its  etiologic  significance  is  not  definitely  determined. 

Ankylostomiasis,  or  Uncinariasis,  is  a  disease  due  to  the  pres- 
ence of  the  hookworm.  11  is  characterized  by  anemia,  which  in 
some  cases  resembles  the  pernicious  type;  the  cells  are  greatly 
reduced  in  number  and  many  nucleated  red  blood  cells  appear. 


Fig.    76. — Cephalic   extremity   of   Uncinaria   Duodenalis.      Profile   and    front   view.      (After 

Leuckart-Gould.) 


Fig.  77. — Duodenum  showing  attached  Uncinaria.     (Specimen  of  Capt.  C.  F.  Kieffer,  U.  S. 
A.,  presented  to  the  Jefferson  Medical  College.) 

The  Lone  marrow  is  pale  and  fatty  or  gelatinous.  The  leucocytes 
are  not  increased,  in  fact  may  he  decreased  but  the  eosinophils 
usually  rise  to  15  or  25  per  cent  of  the  total  leucocytes. 

The  hookworm  attaches  itself  to  the  duodenum  or  upper 
jejunum,  causing  the  loss  of  blood  by  hemorrhage  and  by  ab- 
sorption,  and   produces  hemolysins.     The   patient   becomes   sal- 


204  GENERAL   PATHOLOGY 

low,  debilitated  and  usually  exhibits  epigastric  pain  and  tender- 
ness, with  dyspnea  and  other  symptoms.  Children  become  stunted 
in  growth.  The  disease  prevails  in  tropical  and  subtropical 
countries — India,  Egypt,  Southern  Europe,  West  Indies  and  the 
southern  part  of  the  United  States. 

The  hookworm  or  Ankylostoma  duodenale  is  a  short,  white 
worm — brown  or  red  when  gorged  with  blood — its  head  bent  back 
like  a  hook,  and  its  mouth  having  six  hook-like  teeth.  The  female 
is  10  to  18  x  1  mm.,  the  male  being  about  one-third  smaller,  and 
having  at  its  posterior  end  an  expanded  copulatory  bursa.  The 
ova  when  discharged  incubate  in  moist,  warm  soil  and  the  re- 
sulting larva?  penetrate  the  skin  of  the  feet  of  those  who  work 
in  or  pass  through  the  contaminated  soil.  The  parasite  then 
reaches  the  lungs  and  passes  by  way  of  the  trachea  and  the 
esophagus  into  the  intestines.    (Figs.  76  and  77.) 

The  Necator  Amcrieanus,  or  American,  or  New  World,  Hook- 
worm, is  a  separate  genus,  found  in  the  southern  part  of  the 
United  States,  South  America  and  other  parts.  It  is  smaller  in 
size  and  has  plates  or  suckers  in  place  of  the  hook-like  teeth 
of  the  Old  World  hookworm,  and  its  ova  are  larger,  but  it  has 
practically  the  same  life  history  and  produces  the  same  symp- 
toms and  pathologic  changes. 

Trichinosis  (Trichiniasis)  is  a  parasitic  disease  attended  with 
painful  myositis  and  extensive  edema,  due  to  the  presence  of  the 
larva?  of  the  Trichina  spiralis.  The  larva?  are  ingested  by  those 
who  eat  insufficiently  cooked,  trichinosed  pork.  The  larva?  lie 
curled  and  encysted  in  the  muscles,  where  they  can  remain  alive 
for  many  years,  and  when  ingested  by  man  or  other  animals 
the  capsules  are  digested  and  the  embryonal  worms  liberated. 
They  mature  in  the  small  intestine  where  the  females  (3  to  4 
mm.  long  and  twice  the  size  of  the  males)  are  fecundated,  after 
which  the  males  die.  Within  a  week  1000  to  2000  embryos  are 
born,  which  enter  the  lymph  and  the  blood  streams,  finally  lo- 
cating in  the  muscles  and  become  encysted,  in  which  stage  they 
are  identical  with  the  encysted  stage  in  the  hog.  Hogs  probably 
become  infected  by  eating  offal. 

In  two  or  three  days  after  eating  diseased  meat,  nausea,  vomit- 
ing, pain,  and  diarrhea  usually  occur.  In  the  invasive  stage  there 
is  fever,  and  in  severe  cases  symptoms  resembling  typhoid  fever 


PATHOLOGY    OF     I  N  i'l  :<  "I'll  US    DISEASES 


205 


are  present.  Acute  myositis  with  mild  or  severe  pain  and  in- 
terference with  muscular  function  are  always  aoted,  and  leuco- 
cytosis  with  eosinophilia  constituting  30  to  50  per  cent  of  the 
total  white  cells  is  almost  a  pathognomonic  sign.    The  mortality 

is  5  per  cent,  but  in  certain  epidemics  it  is  much  higher.  (Fig. 
78.) 

Guinea-worm  Disease  (Dracontiasis)  is  a  tropical  disease  due 
to  the  guinea-worm  (dracunculiis  medinensis) .  Man  is  infected 
by  the  Cyclops  (a  minute  fresh-water  crustacean)  and  the  em- 
bryos develop  in  the  intestinal  tract;  after  fecundation  the  male 
dies  and  the  female  enters  the  tissues  through  which  it  slowly 
migrates,  finally  (8  to  16  months)  reaching  the  region  of  the  an- 
kles, where  vesicles  or  ulcers  form,  through  which  the  worm  dis- 
charges her  embryos  periodically,  after  which  it  passes  from  the 


,;-':' 


Fig.    78. — Trichina    spiralis    with    its   connective-tissue    covering:      a,    early    stage;    b,    calci- 
fied.     (Leuckart.) 

body  through  the  same  lesions  and  dies.  The  embryos  enter 
the  cyclops  as  their  intermediate  host. 

Filariasis  is  a  disease  caused  by  various  filaria,  whose  larvae 
are  found  in  the  blood,  while  the  parent  worms  are  found  in 
the  tissues,  the  inner  blood  and  lymphatic  vessels  and  lymph 
glands. 

The  Filaria  bancrofti  (F.  sanguinis  hominis  nocturna)  is  a  white, 
uniformly  cylindrical  worm,  the  female  having  a  curved  tail  and 
the  male  a  spiral  tail.  The  female  gives  birth  to  larva?  (0.3  mm. 
x8ju)  which  pass  into  the  lymph  stream,  thence  into  the  blood 
and  may  be  seen  in  samples  secured  at  night  (or  in  daytime  if 
the  patient  sleeps  during  the  day)  as  small,  snake-like  worms 
whose  active  movements  agitate  the  red  corpuscles.  In  the  day- 
time they  recede  into  the  lungs  and  larger  blood  vessels.  These 
larvae  (microfilaria)  may  remain  in  man  for  years,  being  unable 
to  become  mature  worms  until  they  enter  a  suitable  intermediate 


206 


GENERAL   PATHOLOGY 


host — the  Culex  genus  of  mosquito,  which  may  occur  when  a  pa- 
tient is  bitten  during  a  time  when  the  larva?  are  in  the  peripheral 
blood.  In  the  mosquito  the  larvae  undergo  several  developmental 
changes  and  finally  pass  into  the  proboscis  whence  they  may  be 
inoculated  into  man. 

Pathologically  the  filaria  may  occasion  no  symptoms,  though 
eosinophilia  is  always  present,  but  in  other  cases  the  parent 
worms,  which  lie  curled  up  in  the  larger  lymphatic  vessels,  trunks 
or  even  the  thoracic  duct  cause  obstruction  of  the  vessels,  lead- 
ing to  distention  of  tributary  vessels;  secondary  inflammatory 
thickening  may  occur,  with  distention  and  rupture  of  the  lym- 
phatics of  the  kidneys,  bladder  or  other  structures,  causing 
hematochyluria,  or  of  the  scrotum,  causing  chylocele,  etc.  "When 
very  extensive  the  obstruction  may  extend  to  the  peripheral  lym- 


?M 


-t  ^  ■ 

o 
Q._.       m    - 


Fig.    79. — Filaria   embryo,   alive    in    the   blood.      (F.    P.    Henry.) 

phatics  with  great  distention  of  the  tissues,  known  as  Elephan- 
tiasis, which  usually  affects  the  lower  limbs,  scrotum,  and  less 
often  other  parts.     (Fig.  79.) 

The  Eustrongylus  gigas  is  a  brownish  or  red  worm  (the  female 
may  be  100  cm.  long)  which  is  found  in  the  pelvis  of  the  kidney, 
ureters  and  bladder  of  cattle  and  rarely  of  man,  causing  dilata- 
tion of  these  structures  with  atrophy  of  their  substance. 

Leptus  Autumnalis  is  a  name  applied  to  the  larvae  of  the  harvest 
mite  and  other  mites;  they  possess  a  suctorial  proboscis  with 
which  they  penetrate  the  skin  and  cause  greater  or  less  irrita- 
tion. 

Acarus  scabiei,  or  Itch-mite,  is  a  pale,  spheroidal  body  with 
bristly  legs.  The  male  (0.2  to  0.3  mm.)  lives  upon  the  surface 
of  the  skin,  but  the  female  (0.3  to  0.4  mm.)  after  impregnation 
burrows  into  the  epiderm  (thus  becoming  an  endoparasite  tern- 


PATHOLOGY    OF    INFECTIOUS   DIM    \  207 

porarily)  laying  her  eggs  al  intervals  in  the  epidermal  tunnel, 
which  appears  as  a  dark  line  about  one  centimeter  long,  ami 
oftenest  located  between  the  fingers,  on  the  wrists,  elbows,  axilla?, 
etc.  Vesicles  and  sometimes  pustules  form  along  the  course  of 
the  burrow.  The  ova  hatch  in  a  few  days,  forming  six-legged 
larva;.     (Fig.  80.) 

The  pathologic  manifestations  produced  by  the  Insecta  may  be 
summarized  in  the  statement  that  some  of  them  cause  more  or 


Fig.    80. — Female   acarus    (after   Anderson). 

less  annoyance  by  injecting  an  irritating  salivary  secretion  when 
they  bite,  which  occasionally  causes  eczema,  but  more  often 
leads  to  secondary  bacterial  infection  due  to  the  scratching  in- 
duced by  the  itching. 

The  female  jigger  (Pulex  penetrans)  after  impregnation  bur- 
rows beneath  the  skin,  as  does  the  Acarus  scabiei,  especially  be- 
tween the  toes,  where  she  lays  her  eggs,  causing  inflammation 
and  often  ulceration. 


CHAPTER  IX1 

MALFORMATIONS 

The  term  "malformation"  is  used  to  designate  an  abnormal  de- 
viation from  the  usual  structure  of  parts  or  organs  and  is  the 
result  of  errors  or  accidents  in  the  process  of  development. 

The  study  of  malformations,  therefore,  is  primarily  the  study 
of  embryology,  because  they  occur  during  the  process  of  intra- 
uterine development. 

While  we  have  as  yet  no  classification  that  is  entirely  satis- 
factory, the  following  is  perhaps  the  best  for  the  student. 

1.  Malformations  by  Excess. — The  excess  may  be  simply  a  re- 
dundant foreskin  or  a  supernumerary  digit,  or  it  may  be  an  al- 
most completely  formed  individual  {double  monster).  Gigantism 
also  comes  under  this  head. 

2.  Malformations  by  Defect  include  those  due  to  arrest  of  the 
normal  process  of  development,  and  they  fall  into  three  groups: 

(a)  Those  due  to  defective  development  in  the  posterior  median 
line. 

(b)  Those  due  to  defective  development  in  the  anterior  me- 
dian line,  including  the  structures  of  the  umbilical  cord. 

(c)  Miscellaneous  defects  involving  chiefly  the  internal  or- 
gans. 

3.  Malformations  by  Perversion  include  those  cases  in  which 
the  development  has  been  irregular  or  disorderly. 

Malformations  by  Excess 

In  Double  Monsters  the  duplication  may  be  anything  from  an 
arm  or  leg  to  the  entire  body.  In  the  latter  event,  if  the  de- 
velopment of  the  individuals  is  equal,  two  well-formed  children 
result  {homologous  twins)  ;  but  if  one  is  stronger  than  the  other, 
it  develops  at  the  expense  of  the  weaker,  which  shrivels  up  or 


xThis  chapter  has  been  written  by  J.  Waller  Reeves,  M.D.,  formerly  Trofessor 
of  General  Pathology  in  the  Dental  Department  of  the  University  of  Southern 
California. 

208 


MALFORMATIONS  209 

only  partially  develops.  When  there  are  two  individuals,  they 
are  usually  united  by  corresponding  parts,  and  the  monster  is 
named  according  to  the  location  of  the  union;  For  example,  when 
it  is  at  the  head,  craniopagus;  at  the  sternum,  stemopagus;  at  the 

xiphoid,  xiphopagus  (Siamese  twins);  etc. 

Malformations  by  Defect 

(a)  Malformations  Due  to  Defective  Development  in  the  Pos- 
terior Median  Line. — 

1.  Those  due  to  failure  of  the  neural  groove  to  form  the  neural 
canal. 

(a)  Ancncephalocclc,  in  which  all  the  brain  is  missing. 

(b)  Open  spina  bifiela,  an  absence  of  all  the  structures  covering 
the  medullary  canal. 

These  two  forms  are  incompatible  with  life,  and  of  little  in- 
terest. 

(c)  A  minor  degree  of  spina  bifiela.  These  cases  show  a  tumor 
in  the  lumbar  region,  which  may  contain:  (1)  a  cavity  continuous 
with  the  central  canal  and  surrounded  by  all  the  structures  of  the 
cord  {syringomyelocele)  ;  (2)  part  of  the  cord  with  its  membranes 
(myelonieningocele)  ;  or  (3)  only  the  cord  membranes  (menin- 
gocele). 

(d)  Similar  pouches  in  connection  with  defects  in  the  cranium, 
Avhieh  may  contain  (1)  a  cavity  continuous  with  one  of  the  ven- 
tricles and  surrounded  by  brain  tissue  and  the  membranes  (en- 
eephalocele)  ;  (2)  brain  tissue  and .  membranes  (encephalomenin- 
gocele)  ;  or  (3)  membranes  only  (meningocele). 

2.  Malformations  occurring  after  the  cranium  and  spinal  canal 
are  formed. 

(a)  Microencephalia  (small  brain)  and  micromyelia. 

(b)  Irregular  defects  of  the  cortex. 

(c)  Hydrocephalus,  in  which  there  is  an  abnormal  increase  in 
the  amount  of  fluid  in  the  ventricles  (internal  hydrocephalus)  or 
surrounding  the  brain  (external  hydrocephalus).  The  cranium 
may  reach  an  enormous  size. 

(b)  Malformations  Due  to  Defective  Development  in  the  An- 
terior Median  Line. — 

1.  Irregularities  in  the  fusion  of  the  maxillary  and  nasal  proc- 
esses. 


210 


GENERAL    PATHOLOGY 


Harelip  and  cleft  palate,  which  will  bt  taken  up  in  detail  later. 

2.  Irregularities  in  tht   closing  of  the  branchial  clefts.    Fistula 
in  the  neck. 

3.  Umbilical  ht  rnia. 

4.  Meckel's  diverticulum   is  formed  by  the  persistence   of  the 
omphalomesenteric  duct,  and  is  given  off  from  the  ileum  between 


L           c 

\ 

>4) 

\    B    )               _*i 

j 

V     ^A                 X* 

}     \ 

i 

Fig.  81. 


Fig.   82. 


(After  His.)      C,  frontonasal  process;  B, 


Fig.  81. — Head  of  fetus  at  end  of  fifth  week, 
maxillary  process;  A,  mandibular  processes. 

Fig.  82. — Head  of  fetus  in  the  seventh  week.  (After  His  )  A,  the  now  united  man- 
dibular processes;  B,  the  maxillary  process;  C,  frontonasal  process;  D,  lateral  nasal  proc- 
ess; E,  globular  processes  attached  to  the  nasal  part  of  the  frontonasal  process.  The 
central  nasal  processes  are  separated  from  the  lateral  on  each  side  by  the  lateral  nasal 
grooves,   which   represent   the  anterior  nares. 

12  and  36  inches  from  its  lower  end.    It  is  present  in  about  2  per 
cent  of  persons. 

5.  Yesiced  fistula,  the  bladder  opening  through  the  anterior  ab- 
dominal wall. 

6.  Epispadias,  the  urethra  opening  above  the  penis. 

7.  Hypospadias,  in  which  the  urethral  opening  is  on  the  under 
surface  of  the  penis  or  through  the  scrotum. 

8.  Imperforate  anus. 


MALFORMATIONS 


211 


(c)  Miscellaneous  Defects. — One  or  both  kidneys  may  be  tab- 
ulated or  horseshoe-shaped,  the  testieles  undescended,  viscera 
transposed,  etc. 

The  various  forms  of  clubfoot,  intrauterine  amputations  and 
congenital  hip  dislocation  may  also  he  classed  under  this  head. 

Malformations  of  Perversion  are  too  numerous  and  varied  to 
be  described  in  detail. 


Fig.      84. — Almost    complete    single    harelip 


Fig.    85. — Diagram    of    median    hare- 
lip.      (After    Blair.) 

Harelip  and  Cleft  Palate 

These  malformations  are  due  to  a  failure  of  complete  union 
of  the  maxillary  and  nasal  processes.     (Figs.  81  and  82.) 

Harelip  involves  the  upper  lip,  and  is  usually,  though  not  al- 
ways, complete,  through  the  entire  lip  into  the  nostril.  It  may 
be  single  or  double,  and  is  very  rarely  in  the  median  line.  It 
may  or  may  not  be  associated  with  cleft  palate.  Figs.  83'.  84, 
and  85.) 

Cleft  palate  may  involve  the  soft  palate  only,  or  both  hard 
and  soft  palates,  and  may  be  either  single  or  double.  The  va- 
rious forms  are  shown  in  Figs.  86  and  87. 


212 


GENERAL    PATHOLOGY 


Fig.    86. — Cleft    of    the    hard    and    soft    palate.      (Federspiel.) 


Fig.  87. — Complete  double  cleft  in  an  infant.      (Blair.) 


PART  II 
DENTAL  PATHOLOGY 


CHAPTER  X 
INTRODUCTION 


Dental  pathology  is  the  study  of  dental  and  oral  disease  in  all 
of  its  aspects.  Dental  and  oral  disease  is  any  structural  or  phys- 
iologic deviation  from  the  normal  in  the  hard  tissues  of  the  teeth, 
in  the  pulp,  in  the  peridental  membrane,  in  the  supporting  os- 
seous structures  (i.e.,  the  alveolar  process),  in  the  gingivae  and 
gums,  in  the  soft  tissue  lining  of  the  mouth,  and  in  the  salivary 
glands. 

The  study  of  the  anatomic  changes  in  cells,  as  the  results  of 
disease-producing  influences,  is  concerned  with  morbid  anatomy 
and  morbid  histology,  or  as  generally  termed,  pathologic  anatomy. 
The  study  of  altered  function  resulting  from  abnormal  degrees 
of  irritation  of  any  kind  is  concerned  with  morbid  or  pathologic 
physiology.  We  shall  endeavor  throughout  the  book  to  discuss 
dental  diseases  from  both  viewpoints. 

The  conditions  giving  rise  to  disease,  whether  predisposing  or 
exciting,  are  included  in  the  study  of  etiology,  which  has  refer- 
ence to  the  cause,  or  group  of  causes  which  give  rise  to  ana- 
tomic or  physiologic  deviations  from  the  normal. 

Predisposing  and  Exciting  Causes 

If  man  were  to  live  a  better  regulated  life  than  is  generally 
possible  in  this  age  of  intense  physical  and  mental  needs,  par- 
ticularly so  in  regard  to  proper  diet,  clothing,  ventilation,  ex- 
ercise, rest,  both  physical  and  mental,  and  sleep — doubtless  the 
toll  of  disease  would  be  much  less  than  is  actually  the  case.  The 
functions  of  the  tissues  and  organs  of  the  body  would  be  car- 

213 


214  DENTAL    PATHOLOGY 

ried  on,  after  the  stage  of  maturity  had  been  reached,  in  such 
a  way  as  to  make  up  for  functional  disuse  without  undue  stress 
on  any  of  the  body  structures,  and  this  state  of  functional  balance 
would  be  accompanied  by  the  expression  of  a  maximum  of  power 
on  the  part  of  the  cells  and  fluids  of  the  body  to  resist  bacterial 
infection.  The  vital  resistance  would  be  at  its  highest.  As  it  is, 
the  degree  of  vital  resistance  varies  frequently,  at  times  being 
high  (i.e.,  nonreceptivity  to  bacterial  infections),  and  at  others 
below  par,  or  low  (i.e.,  receptivity  to  bacterial  infection).  A  de- 
gree of  vital  resistance  below  the  maximum  for  a  given  individual 
predisposes  to  and  makes  possible  the  onset  of  disease. 

Lowered  Vital  Resistance 

The  conditions  which  lower  vital  resistance  are  improper  cloth- 
ing, extremes  of  temperature,  errors  of  diet  in  either  quantity 
or  quality  of  food,  faulty  metabolism  (defective  assimilation, 
elimination  or  both),  excessive  use  of  alcoholic  beverages,  poor 
ventilation  of  living  quarters,  continued  dampness,  mechanical 
and  thermal  irritation,  foci  of  chronic  infection,  chemical  poisons, 
addiction  to  drug  forming  habits,  anatomic  abnormalities,  men- 
tal depression,  etc.  In  the  presence  of  any  one  or  more  of  the 
foregoing  conditions  the  power  of  the  human  organism  to  ward 
off  a  bacterial  invasion  is  minimized,  and  the  microorganisms 
which  first  enter  any  portion  of  the  body,  being  enabled  to  prop- 
agate the  infection  soon  acquires  a  degree  of  virulence  which 
is  manifested  in  various  kinds  and  degrees  of  cell  degeneration 
or  death.  Vital  resistance  below  par  renders  the  individual  sus- 
ceptible to  disease. 

Exciting  Causes 

"While  some  of  the  conditions  enumerated  under  the  heading  of 
predisposing  causes  play  an  important  role  in  the  development 
of  disease  of  bacterial  origin,  it  is  to  be  borne  in  mind,  however, 
that  there  are  diseases  whose  etiology  can  not  be  directly  as- 
sociated with  the  presence  of  bacteria.  It  is  then  that  abnormal 
food  supply,  sudden  extremes  in  temperature,  mechanical  forces, 
chemical  poisons,  congenital  anatomic  deviations,  and  changes 
in  the  external  or  internal  secretions — all  of  these  without  bac- 
terial infection,  have  to  be  included  in  the   group  of  exciting 


INTRODUCTION  215 

causes.  Thai  is  to  say,  any  one  or  more  of  the  nonbacterial 
factors  may  incite  a  diseased  state  regardless  of  any  bacterial 
activity.  In  the  so-called  diseases  of  metabolism,  for  instance, 
pathogenic  bacteria  are,  strictly  speaking,  no1  concerned,  and 
it'  concerned,  are  secondary  to  the  primary  etiologic  causes.  The 
condition  of  1  lie  individual  will  depend  upon  the  normal  or  ab- 
normal assimilation  of  f 1.  this  being  governed  by  the  quality 

and  quantity  of  the  digestive  secretions.  Again,  pathogenic 
bacteria  are  excluded  as  causative  factors  in  such  pathologic  con- 
ditions as  rickets,  myxedema,  cretinism,  exophthalmic  goiter, 
Addison's  disease,  hyperglycemia,  diabetes,  arteriosclerosis,  val- 
vular disorders,  i 

Predisposing'  Causes  of  Dental  Disease 

In  diseases  of  the  teeth  and  associated  structures,  the  predispos- 
ing cause  may  be  found  in  an  impairnu  nt  of  circulatory  activity. 
This  is  often  brought  about  by  the  existence  of  a  systemic  dis- 
order. Consequently,  that  which  from  the  standpoint  of  the  phy- 
sician is  the  manifestation  of  an  exciting  cause — disease — from 
that  of  the  dentist  it  must  be  considered  as  the  predisposing  cause 
of  the  dental  and  oral  disorder.  We  know,  for  instance,  that 
after  the  removal  of  all  sources  of  irritation  to  the  peridental 
membrane,  alveolar  process,  and  gingivae  in  a  case  of  true  pyor- 
rhea alveolaris,  not  infrequently  the  pathologic  process  con- 
tinues. The  structures  concerned  at  no  time  develop  the  max- 
imum of  vital  resistance  necessary  to  overcome  the  bacterial  ele- 
ment concerned  in  the  process.  This  lessened  resistance  in  the 
supporting  tissues  may  be  the  result  of  abnormal  circulation  fol- 
lowing, for  instance,  some  error  of  metabolism.  This  would  be 
caused,  for  example,  by  the  presence  in  the  stomach  of  an  in- 
sufficient amount  of  hydrochloric  acid  (hypochlorhydria).  From 
the  physician's  standpoint  hypochlorhydria  is  the  exciting  or 
direct  cause  of  the  digestive  disorder  to  which  it  has  given  rise, 
while  from  the  dentist's  standpoint,  hypochlorhydria  is  only  the 
predisposing  cause  of  the  dental  disorder,  for  the  reason  that  it 
has  brought  about  errors  of  metabolism  which  prevent  the  de- 
velopment of  a  sufficient  degree  of  vital  resistance  in  the  in- 
vesting tissues  of  the  teeth  and  retard  or  prevent  the  eradication 
of  the  infectious  processes  around  the  teeth.     Any  systemic  con- 


216  DENTAL   PATHOLOGY 

dition  which  is  a  deviation  from  the  normal,  and  which  is  the 
result  of  a  combination  of  exciting  causes,  may  become  the  pre- 
disposing cause  of  a  dental  or  oral  disease. 

Disease,  general  or  dental,  itself  is  not  a  separate  entity,  out  may 
be  defined  as  abnormality  in  structure,  in  function,  or  in  both  com- 
bineel.1 

The  general  division  of  disease  into  organic  and  functional,  im- 
plying in  the  former  case  alteration  of  cellular  structure,  and 
in  the  latter  alteration  of  physiologic  function  without  alteration 
of  structure,  is  of  doubtful  value  in  its  application  to  general  dis- 
ease and  to  dental  and  oral  disease.  It  is  true  that  physiologic 
derangement  may  exist  without  any  apparent  structural  changes, 
but  then  it  is  more  probable  that  cellular  changes  have  taken 
place  which  it  is  not  possible  to  locate  and  analyze  because  of 
as  yet  a  relatively  imperfect  pathologic  technic.  The  conception 
of  modern  pathology,  general  and  dental,  is  almost  exclusively 
anatomic,  i.e.,  structural  changes  in  the  cells.  The  changed  ap- 
pearance of  an  organ  which  results  from  the  changes  in  its  cells; 
the  study  of  the  retrograde  changes  in  the  cells  themselves  by 
means  of  the  microscope;  the  changes  in  the  body  secretions;  the 
nature  of  the  body  excretions — these  are  some  of  the  most  im- 
portant phases  in  the  study  of  pathology,  whether  general  or 
dental.     Gross  pathology  studies  macroscopic  changes  only. 

Prior  to  the  promulgation  of  the  cell  theory  of  disease,  the 
study  of  pathology  consisted  almost  exclusively  in  the  observa- 
tion of  gross  anatomic  changes,  and  in  the  manifestations  of 
pathologic  physiology.  The  conclusion  that  disease  is  the  result 
of  the  sum  total  of  the  changes  which  take  place  in  the  individual 
cells  consecpient  upon  the  continued  influence  of  irritation,  ab- 
normal in  character  or  amount,  marks  the  beginning  of  a  logical 
conception  of  general  and  dental  pathology. 


1Stengel  and   Fox:     Text-book  of   Pathology,   Philadelphia,   W.   B.    Saunders. 


CHAPTER  XI 
ENAMEL,  DENTIN,  AND  CEMENTTJM 

Normal  Histologic  Considerations 

It  being  impossible  to  appreciate  deviations  in  the  substance 
of  the  enamel,  dentin,  or  cementum, — the  hard  tissues  of  the 
teeth — in  the  pulp,  or  in  the  bony  or  soft  investing  structures, 
without  previous  clear  conceptions  of  these  tissues  when  within 
the  limits  of  normality,  it  becomes  advisable  to  review  the  his- 
tology of  all  of  them  beginning  with  that  of  the  enamel.  We 
shall  consider  also  the  relation  of  the  latter  to  the  dentin  and 
cementum,  bearing  in  mind  that  the  study  of  the  normal  charac- 
teristics of  these  tissues  is  undertaken  as  a  means  of  facilitating 
the  comprehension  of  the  pathologic  processes  which  may  con- 
cern them. 

Normal  Enamel 

The  enamel,  the  hardest  tissue  of  the  body,  is  a  specialized 
form  of  calcined  epithelial  tissue  of  ectodermic  origin,  which 
surrounds  the  crown  of  the  tooth  in  its  entirety  and  extends  to 
the  gingival  line.  Here  it  is  covered  by  the  unattached  gingiva? 
for  a  distance  of  several  millimeters.  It  varies  in  thickness  from 
the  gingival  line,  where  it  is  the  thinnest,  to  the  occlusal  or  in- 
cising edges  where  it  is  the  thickest.  The  increase  in  thickness 
is  gradual  and  particularly  Avell  marked  at  such  areas  of  the 
tooth  as  arc  usually  subjected  to  strong  and  continued  friction  and 
stress  during  mastication.  The  greater  the  stress  to  which  an  area 
of  crown  surface  is  subjected,  the  thicker  and  more  resistant  will 
be  the  enamel  on  such  an  area,  not  because  of  any  difference  in 
chemical  composition,  but  because  of  a  peculiar  arrangement  of 
the  enamel  rods  to  meet  the  requirements  of  great  stress.  Per- 
fection in  development  throughout  the  enamel  is  rarely  encoun- 
tered so  that  in  describing  this  tissue  our  aim  will  be  to  describe 
the  microscopic  appearance  of  an  average  specimen  falling  within 
the  limits  of  normality.     (Figs.  88  and  89.) 

217 


218 


DENTAL    PATHOLOGY 


Fig.   SS. — Area   of   normal   dentin   and   enamel,     a,   dentin;    b,   enamel;    c,    c',   dentoenamel 
junction;   e,  dentinal   tubuli;  /,   series  of  interglobular   spaces  faintly   reproduced. 


ENAMEL,    DENTIN,    AND    CEMENT!    M 


219 


The  components  <>!'  enamel  are  the  enamel  rods  and  the  confut- 
ing or  interprismatic  substance,  the  latter  being  the  binding  ma- 
terial which  holds  the  rods  together.  This  substance,  like  the 
enamel  rods,  of  ectodermic  origin,  is  a  calcified  stratified-squa- 

limus  epithelium.  The  rods  are  five-  or  six-sided  and  from  three 
and  one-half  to  four  and  one-half  microns  in  Length.  Some  of 
the  rods  may  he  traced  from  the  dentoenamel  junction  to  the 
surface  of  the  crown  of  the  tooth.     The  cementing  substance  is 


Fig.  89. — Area  of  normal  dentin  and  enamel  from  ground  section  of  area  near  apex 
of  incisor  of  man.  a,  dentin,  showing  dentinal  tubules;  b,  enamel;  c,  crack  in  enamel 
made   in   grinding. 


more  susceptible  to  the  action  of  dilute  acids  than  the  enamel 
rods,  so  that  if  a  section  of  enamel  be  subjected  to  dilute  hy- 
drochloric or  lactic  acid,  until  the  cementing  substance  is  in  part 
dissolved,  a  clear  differentiation  between  enamel  rods  and  ce- 
menting substance  will  be  obtained.  This  is  due  to  the  fact 
that  upon  the  removal  of  the  cementing  substance  a  greater  dif- 
ference in  the  indices  of  refraction  of  the  enamel  rods  and  the 
decreased  cementing  substance  between  them  will  have  been  es- 


220 


DENTAL    PATHOLOGY 


tahlished  Fiy.  DO...  Examination  of  a  ground  section  of  a  tooth 
with  a  16  mm.  objective  does  not  render  possible  the  detection 
of  the  physical  peculiarities  of  the  individual  rods  or  of  the  ce- 
menting substance.  With  a  higher  magnification,  in  a  longi- 
tudinal section  the  individual  rods  appear  as  a  series  of  striations 
of  alternating  dark  and  light  areas.  It  is  with  difficulty  that  a 
rod  can  be  traced  microscopically  from  its  free  end  to  the  dento- 
enamel  junction.  Upon  the  axial  surfaces  the  rods  are  more  or 
less  parallel  to  each  other  and  mosl  of  them,  according  to  Noyes, 
extend  from  the  dentin  to  the  free  surface  of  the  enamel.1     That 


'Hl^k. 


.6 


Fig.   90.— Contrast  between  norma!  enamel  at  a  and  a' ',  and  decalcified  enamel  at  b  and  b'. 

they  extend  as  single  rods  to  the  free  surface  of  the  enamel  must 
he  concluded  largely  from  observation  in  cleaving  enamel  in 
the  preparation  of  cavities  for  the  reception  of  fillings.  Mi- 
croscopically  ii  is  practically  futile  to  attempt  to  trace  the  rods 
across  the  section  as  single  rods.  The  majority  (_,i'  sections  that 
have  been  examined  })y  the  author  show  the  tendency  toward 
parallelism  of  the  rods  on  the  axial  surfaces,  but,  on  the  other 
hand,  do  not  show  many  rods  traceable  uninterruptedly  from 
within  to  the  free  surface  of  the  enamel  (Fig.  91). 

Woyes:      Dental    Histology   and    Embryology,    Philadelphia,    Lea   &    Febiger. 


ENAMEL,    DENTIN,    AND    CEMENTUM 


221 


Another  peculiarity  of  enamel,  within  the  bounds  of  nor- 
mality arc  the  bands  of  Betzius.  These  are  better  seen  upon  ex- 
amination with  a  low-power  objective  and  appear  as  brownish 
striations  which  mark  the  beginning  and  completion  of  the  cal- 
cification of  sections  of  enamel  structure.  They  are  the  boundary 
lines  between  calcification  installments,  and  hence  have  been  ap- 
propriately   named    by    the    descriptive    term    incremental    Inns 


b' 


Fig.  91. — Ground  section.  Dentoenamel  junction.  The  character  of  the  granular 
layer  of  Tomes  is  unusually  well  shown.  The  hearing  which  this  laver  has  upon  the 
progress  of  caries  should  not  be  overlooked.  This  section  also  shows  the  tendency  at 
parallelism  of  the  enamel  rods;   a,  a',  enamel;   b.b',  dentin;   c,  c' ,  granular  layer. 

(Noyes).  The  portions  of  enamel  included  between  the  dento- 
enamel junction  and  a  hand  of  Retzius,  and  between  the  bands 
themselves,  represent  synchronous  calcification  installments  (Fig. 
92).  These  bands  of  brownish  color,  when  viewed  under  a  low 
or  high  amplification,  run  obliquely  across  the  lengths  of  the 
enamel  rods  from  the  dentoenamel  junction  on  one  side  to  the 


222 


DENTAL   PATHOLOGY 


dentoenamel  junction  on  the  opposite  (from  mesial  to  distal  sur- 
faces) in  the  incisal  region  and  in  the  cusps  of  bicuspids  and 
molars.  Beyond  these  regions  they  run  from  the  dentoenamel 
junction  to  the  surface  of  the  enamel.  They  mark  the  strata  of 
enamel  in  the  order  of  their  calcification.  They  begin  at  the 
dentoenamel  junction  in  the  region  of  the  incisal  area,  and  ter- 

a 


-d' 


J 


I 


c 


Pig.  92. — Ground  section,  longitudinal,  showing  the  prevailing  mode  of  junction  of 
enamel  and  cementum.  Inasmuch  as  the  calcification  of  the  enamel  is  completed  before 
that  of  the  cementum  begins,  the  latter  tissue  either  overlaps  the  enamel  or  the  joint  is 
of  the  butt  type.  The  lines  of  Retzius  are  also  seen.  a.  a',  dentin;  b,b',  enamel;  c,  c' , 
cementum.  In  the  enamel  the  lines  running  obliquely  from  the  dentin  to  the  free  sur- 
face of  the  enamel  are  the  lines  of  Retzius  d,  d' ;  line  of  junction  between  enamel  and 
cementum,   the  latter  overlapping  the  enamel,  seen  at  c. 

minate,  after  following  a  curved  course,  at  some  other  point  in  the 
dentoenamel  junction. 

Sections  of  enamel  when  examined  under  a  low  power  with 
direct  light  occasionally  exhibit  markings  or  bands  running  at 
right  angles  to  the  dentin.  These  are  the  lines  of  Shreger  and 
are   due   to   "alternating  uniform   curvatures   of  the   prismatic 


ENAMEL,    DENTIN,    AND    CEMENTUM 


223 


bundles."  They  embody  no  significance,  histologic  and  path- 
ologic. 

Recently  Lodge2  lias  made  an  interesting  study  of  the  cause  of 
the  presence  of  these  lines,  lie  has  found,  by  superimposing  two 
wire  screens  and  viewing  them  over  a  white  surface  or  by  sub- 
dued transmitted  light  or  by  placing  together  two  layers  of  a 
silk  fabric,  that  the  lines  of  Shreger  can  be  simulated.  The  lines 
of  Shreger  are  due,  according  to  Lodge,  to  "net"  effects  pro- 
duced by  light  falling  upon  the  cut  enamel  prisms,  the  optical 
densities  varying  according  as  the  meshes  of  these  nets  are  in 
apposition  or  in  interference.  The  lines  are  difficult  to  see  where 
the  section  is  cut  absolutely  parallel  to  the  long  axis  of  the 
enamel  rods,  but  are  plainly  observable  when  sections  of  the 
same  enamel  are  made  at  45°  or  more  to  the  first-made  sections. 

Chemically,  the  enamel  is  composed  mainly  of  salts  of  calcium, 
with  a  trace  of  salts  of  magnesium,  and  other  salts  in  smaller 
proportions.    This  may  be  outlined  as  follows : 

Calcium  phosphate  and  fluoride         89.82% 
Calcium   carbonate  4.37% 

Magnesium   phosphate  1.34% 

Other  salts  .88% 

Organic  matter  3.59% 

100%' 

It  possesses  a  peculiar  luster,  to  which  it  owes  its  names.  The 
word  enamel  is  derived  from  the  old  French  word  esmail,  this  in 
turn  being  derived  from  the  Latin  smaltum,  a  term  first  given  to 
a  vitreous  compound  when  fused  upon  a  metallic  surface. 

The  surfaces  of  the  enamel  upon  all  the  aspects  of  the  tooth 
are  not  normally  smooth,  but  on  the  contrary  the  enamel  is 
"traversed  on  its  vertical  aspect  by  minute  ridges  separated 
from  each  other  by  corresponding  'furrows'  which  run  parallel 
to  each  other  in  a  direction  at  right  angles  to  the  long  axis  of 
the  tooth.  These  horizontal  lines  are  in  some  cases  large  enough 
to  be  visible  to  the  naked  eye,  and  must  have  been  noticed  oc- 
casionally by  many  who,  like  myself  [Pickerill],  thought  at  first 
that  they  were  either  caused  by  attrition  or  were  a  microscopic 
form  of  hypoplasia."3 

=Lodge.  E.   Ballard:     Dental  Cosmos,  lix,   1087.  _       „,.,,,..       r,     o 

3Pickerill:  The  Prevention  of  Dental  Caries  and  Oral  Sepsis,  Philadelphia,  b.  b. 
White  &  Co. 


224 


DENTAL   PATHOLOGY 


This  investigator  has  named  these  horizontal  lines  "the  imbri- 
cation lines  of  the  enamel"  (Figs.  93  and  94).  These  horizontal 
lines  are  widest   and   the   furrows  between  them   deepest  at   a 


Fig.   93.    -Imbrication  lines  on  lower  incisor  of  sclerotic  type   (Pickerill.) 


Fig.   94. — Imbrication    lines    on    lower   incisor   of   malacotic    type    (Pickerill.) 

point  two-thirds  the  distance  from  the  neck  of  the  tooth  to  the 
cutting  or  occlusal  surface.  In  the  teeth  of  the  uncivilized  races 
in  which  dental  caries  is  so  much  less  frequent  than  in  the  teeth 
of  the  modern  races,  the  imbrication  lines  are  less  marked.     In 


ENAMEL,    DENTIN,    A.ND    CEMENTUM 


225 


fact,  he  says,  the  enamel  of  the  teeth  of  the  primitive  races  is 
more  lustrous,  and  the  imbrication  Lines  arc  so  feeble  that  they 
.•an  qo1  be  brough.1  out  by  the  graphite  method  of  staining.  In- 
asmuch as  the  more  susceptible  to  caries  a  tooth  is,  the  more 
marked  arc  the  imbrication  lines  and  the  deeper  are  the  fur- 
rows between  them,  the  conclusion  is  reached  that  the  character 
of  the  external  surface  of  the  enamel  as  to  the  presence  of  mi- 
croscopic <ni<l  macroscopic  unevennesses  is  one  among  many  factors 
which  determines  the  susceptibility  of  the  tooth  to  dental  caries.  The 
less  smooth  the  surface  of  the  enamel,  the  more  difficult  it  be- 
comes to  maintain  these  surfaces  free  from  food  deposits,  saliva 


Pig.   95_ — Calcarine    fissures   on   the   surface   of  a  malacotic   molar    (Pickerill). 


or  salivary  mucin.  In  addition  to  these  imbrication  lines  upon 
the  surface  of  the  enamel  which  are  apparently  external  mani- 
festations of  the  thickness,  the  uneven  lengths  and  number 
of  the  bands  of  Retzius,  the  enamel  also  presents  fissures  which 
are  short  and  numerous,  and  which  run  more  or  less  at  right 
angles  to  the  horizontal  imbrication  lines.  These  should  be  des- 
ignated as  "Picket-ill's  calcarine  fissures."  They  are  present  in 
greatest  numbers  on  the  mesial  and  distal  surfaces  and  on  those 
points  Avhere  the  ridges  are  most  marked,  i.e.,  at  a  point  one-half 
the  distance  between  the  cervix  and  the  occlusal  surface  (Fig. 
95) .  Shallow  long  fissures  and  deep  fissures,  which  may  run  either 
parallel  with  or  at  right  angles  from  the  long  axis  of  the  tooth, 


226  DENTAL   PATHOLOGY 

are  also  present  in  the  teeth  of  the  modern  races  susceptible  to 
dental  caries  and  are  etiologic  factors  in  the  frequency  of  caries 
in  these  races;  and  vice  versa,  their  absence  from  the  enamel 
of  the  teeth  of  the  primitive  races  accounts  to  some  extent  for 
their  nonsusceptibility  to  caries. 

The  question  of  the  comparative  hardness  of  teeth  has  been  for 
many  years  the  subject  of  contradictory  conclusions  on  the  part 
of  investigators  and  clinicians,  the  latter  tenaciously  adhering  to 
the  observations  that  from  the  standpoint  of  resistance  to  the 
cutting  edge  of  instruments  or  to  the  revolving  dental  bur,  the 
enamel  and  dentin  in  different  teeth  in  the  same  mouth,  or  in 
different  mouths,  are  not  of  the  same  degree  of  hardness.  The 
conclusions  of  G.  V.  Black4  are  that  the  clinicians'  classification 
of  teeth  into  hard  and  soft  is  untenable  in  the  light  of  his 
findings  on  the  calcium  salt  content  of  teeth  which  decay  badly, 
and  of  those  which  are  immune  to  caries.  He  says  that  "teeth 
that  decay  badly  have  just  as  much  calcium  salts,  are  just  as 
heavy  and  just  as  hard  as  teeth  of  persons  immune  to  caries," 
but  this  must  be  modified  to  some  extent  on  the  face  of  the  find- 
ings and  conclusions  of  Pickerill.  In  order  to  secure  a  clear  idea 
of  the  position  assumed  by  the  latter  investigator,  it  becomes  nec- 
essary to  establish  a  difference  between  the  specific  gravity  of  the 
enamel  and  its  mass  density.  The  fact  that  from  any  number 
of  specimens  the  enamel  is  of  the  same  specific  gravity,  is  no 
guarantee  that  the  mass  density  of  the  different  specimens  is 
likewise  unvarying.  The  specific  gravity  of  individual  enamel 
rods  may  be  the  same,  but  the  mass  density  of  the  caps  of  enamel 
seems  to  vary  as  between  teeth  which  decay  readily  and  those 
which  do  not.  Thus  the  mass  density  of  the  enamel  of  "native" 
teeth  (teeth  of  the  uncivilized  tribes  least  susceptible  of  all  to 
the  ravages  of  caries)  was  found  to  be  2.858;  that  of  so-called 
hard  (sclerotic  teeth),  2.821;  and  that  of  so-called  soft  (malacotic) 
teeth,  2.723. 5  These  differences  in  density  are  apparently  due  to 
differences  in  the  porosity  of  the  enamel  even  in  the  presence  of 
an  unvarying  specific  gravity  of  individual  enamel  rods  or  groups 
of  rods.  The  differences  in  porosity  account  for  the  various 
degrees  of  permeability  of  the  enamel  at  different  ages  in  the 


4Black,  G.   V.:     Dental  Cosmos,  xxxvii,  353. 
5Pickerill:  Loc.  cit. 


ENAMEL,    DENTIN,    AND    CEMENTUM 


227 


same  teeth  and  in  teeth  from  different  mouths.  Thus,  as  re- 
corded by  Pickerill,  the  permeability  of  the  enamel  decreases 
with  the  age  of  the  tooth;  or,  the  shorter  the  time  elapsed  since 
the  day  of  eruption,  the  more  permeable  the  tooth,  and  vice 
versa.  Likewise,  the  less  the  age  of  the  tooth,  the  smaller  is  its 
mass  density;  and  the  greater  the  age  of  the  tooth,  the  greater  is 


Fig.  96. — Decalcified  longitudinal  section  showing  butt  type  of  enamel-cementum 
junction  at  a.  Some  of  the  enamel  rods  at  b  are  seen  to  run  uninterruptedly  from  the 
dentoenamel  junction  to  the  free  surface.  The  primary  curves  of  the  dentinal  tubules 
at  the  dentoenamel  junction  carry  out  the  arrangement  so  frequently  prevailing,  viz.,  the 
convex  outline  of  the  curvature  is  toward  the  root,  and  the  concave  toward  the  incisal  or 
occlusal    surface. 


its  mass  density.  Pickerill  sees  a  direct  relation  between  the  per- 
meability of  the  enamel  and  the  effects  of  acids.  In  fact  the  com- 
parative tests  show  greatest  destructiveness  by  acids  in  just  those 
teeth  and  at  just  such  times  as  the  porosity  of  the  enamel  is  most 
marked  and  the  density  proportionately  less  marked. 


228  DENTAL   PATHOLOGY 

The  unvarying  hardness  of  the  enamel  of  all  teeth — one  of 
Black's  conclusions — is  likewise  questioned  by  Pickerill  on  the 
basis  that  the  more  reliable  methods  of  determining  the  hardness 
of  various  substances  by  scratching  were  not  then  employed. 
Pickerill  has  used  in  these  experiments  an  ingenious  device  of 
his  invention,  the  selerometer.  by  means  of  which  "the  tooth 
to  be  examined  is  made  to  glide  under  a  diamond  point  which  is 
attached  to  an  accurately  balanced  brass  rod.  The  rod  beyond 
the  point  is  graduated  in  centimeters  and  millimeters,  and  on 
the  rod  slides  a  5-  or  10-gram  weight.  By  altering  the  position 
of  the  weight  on  the  rod.  an  increasing  amount  of  pressure  can 
be  made  on  the  diamond  point;  and  since  the  weight  is  known 
and  the  distance  is  known,  it  is  a  simple  matter  to  calculate  the 
actual  pressure  upon  the  point  for  any  setting.  The  method 
adopted  was  to  draw  the  tooth  under  the  point  with  gradually 
increasing  pressures  until  in  the  enamel  a  scratch  was  made  which 
could  be  distinctly  seen  with  the  naked  eye  when  rubbed  with 
graphite.  A  series  of  teeth  examined  in  this  way  by  the  same 
observer,  with  the  same  diamond  point  and  at  the  same  time 
of  day.  supports  his  contention  that  there  is  a  difference  in  the 
hardness  of  different  enamels,  and  that  this  difference  exists  be- 
tween so-called  hard  (sclerotic)  teeth,  and  soft  (malacotic) 
teeth."6 

The  line  of  junction  between  the  enamel  and  the  cementum 
is  either  one  in  which  the  cementum  overlaps  the  enamel  (Fig.  92) 
or  else  one  in  which  the  two  tissues  form  a  butt  joint   (Fig.  96). 

Dentin 

The  dentin  forms  the  bulk  of  the  tooth  (Fig.  97)  being  covered 
by  the  enamel  in  the  crown  portion  of  the  tooth  and  by  cementum 
in  the  root  portion.  Even  after  the  removal  of  the  enamel,  the 
outlines  of  the  mass  of  dentin  follow  the  general  shape  of  the 
crown  and  root  of  the  tooth.  It  is  a  specialized  form  of  cal- 
cified connective  tissue  of  mesodermic  origin — a  glue-giving  sub- 
stance— composed  of  minute  channels,  the  dentinal  tubules,  from 
1.3  to  2.5  microns  in  diameter  (Figs.  98  and  99),  these  containing 
the  dentinal  fibrilla   which  are  the  protoplasmic  prolongations  of 


'From  the  pathologic  standpoint  the  investigations  of  Pickerill  on  the  physical  ami 
chemical  properties  of  human  enamel  are  of  untold  value:  for  a  complete  survey  of  the 
question   the  reader   is    referred    to   the   original   work.      (Pickerill,    II.    I'.:     Loc.    cit.) 


Fig.  97. — Longitudinal  section  of  upper  cuspid  showing  the  course  and  arrangement 
of  the  dentinal  tubuli.  The  arrangement  of  the  enamel  rods  and  the  anastomosis  of  the 
tubuli  at  the  dentoenamel  junction  are  seen.  This  picture  is  from  a  pen  and  ink  drawing 
of  a  ground  section  which  did   not  involve  the  root  canal   in  its  entirety. 


EN  Will..    DENTIN,    A\l>    CEMENTUM 


L'L'M 


Fig.  98. — A  field  of  dentinal  tubules.    At  a,  b,  and  c  individual  tubules  are  plainly  visible. 


Fig.  99. — Transverse  section  of  dentin.     The  dentinal  tubules  are  cut  somewhat  diagonally. 


230  DENTAL    PATHOLOGY 

the  odontoblastic  layer  of  the  pulp;  of  a  matrix,  the  dentin  matrix, 

or  substance  occupying  the  spaces  between  the  tubules;  and  of  the 
sheaths  of  Newman,  which  may  be  sheaths  of  the  fibrillae  lying  in 
apposition  with  the  tubular  wall  or  a  substance  more  resisting 
to  acids  than  the  dentin  matrix,  and  located  immediately  outside 
the  tuhuli.  The  substance  which  makes  up  the  sheaths  of  New- 
man is  probably  elastin,  soluble  only  in  concentrated  acids  or 
caustic  alkalies,  but  digestible  by  bacterial  ferments. 

Dentin  is  hard,  though  elastic,  usually  of  a  yellowish  white 
color  and  of  a  slight  degree  of  translucency.  In  the  crown  por- 
tion of  the  dentin  the  tubuli  run  a  wavy  course  from  the  dento- 
enamel  junction  to  the  walls  of  the  pulp  chamber,  and  being 
disposed  everywhere  in  a  more  or  less  perpendicular  direction 
to  the  external  surface  of  the  tooth,  radiate  in  various  directions. 
In  the  root  portion  of  the  dentin  they  run  for  a  distance  only, 
an  almost  straight  course  at  practically  right  angles  to  the  long 
axis  of  the  tcoth.  but  as  the  apical  third  of  the  root  is  approached, 
their  direction  becomes  apical  and  a  radial  effect  is  produced. 
The  diameter  of  the  tubules  is  greater  on  the  pulp  end  than  on 
the  enamel  or  cementum  end  and  are  in  closer  proximity  to  each 
other  where  they  are  the  wider  in  diameter.  The  tubules  anas- 
tomose with  one  another,  these  anastomoses  being  more  marked 
in  the  root  than  in  the  crown.  In  the  incisors,  in  the  middle  of 
the  incisal  region  of  the  crown,  the  tubules  run  a  course  almost 
parallel  with  the  long  axis  of  the  tooth,  maintaining  this  for  a 
short  distance  toward  the  mesio-incisal  and  disto-incisal  angles. 
They  then  assume  a  course  which  becomes  less  and  less  oblique, 
until  the  junction  of  the  lower  with  the  middle  third  of  the  root, 
where  the  course  of  the  tubules  is  practically  at  right  angles  to 
the  long  axis  of  the  tooth.  The  tubules  follow  the  same  relative 
direction  upon  the  labial  and  lingual  and  mesial  and  distal  as- 
pects of  the  tooth  in  its  entire  length.  In  the  incisal  region,  if 
a  mesiodistal  section  be  examined,  the  tubuli  will  be  found  to 
run  from  the  dentoenamel  junction  toward  the  pulp  chamber  in 
a  fan-like  arrangement. 

In  molars  and  bicuspids  the  tubules  form  an  arrangement 
something  like  this:  Beginning  at  the  enamel-cementum  junction 
and  toward  the  occlusal  aspect  the  tubules  sweep  toward  the  pulp 
chamber  describing  a  double  curve.     The  curve  near  the  dento- 


ENAMEL,    DENTIN,    AND    CEMENTUM 


231 


enamel  junction  presents  its  convex  surfi toward  tlie  occlusal 

and  its  concave  surface  inward  the  apex.  The  curve  a1  the  rool 
canal  wall  is  less  marked,  the  concave  aspect  being  directed 
toward  the  occlusal  and  the  convex  toward  the  apex.  The  tubules 
in  relation  to  the  cusp  present  a  typical  wheat-sheaf  arrangement. 
The  granular  layer  of  Tomes,  so-called  because  of  its  having  been 


Fig.  100. — Interglobular  spaces  of  Czerrr.ack  in  the  dentin.  Evidences  of  periods  of 
arrestment  of  calcification  of  the  dentinal  tubules.  The  presence  of  a  large  number  of 
these  spaces  would  render  more  rapid  the  progress  of  caries  in  the  areas  in  which  they 
are  located,  by  reason  of  the  greater  penetrability  of  the  tissue  to  the  acid  end  products 
of  fermentation,     a,  a',  a",  interglobular  spaces  of  Czermack. 

first  described  by  Sir  John  Tomes,  represents  a  system  of  inter- 
communication among  the  tubules  at  the  dentin-cementum  and 
dentoenamel  lines.  It  is  more  marked  at  the  dentin-cementum 
line  than  it  is  in  the  crown  portion  of  the  tooth.  These  spaces, 
produced  by  the  widening  out  of  the  tubules,  are  filled  with  pro- 
toplasmic matter  and  are  responsible  for  the  increased  sensitive- 


232 


DENTAL    PATHOLOGY 


ness  of  dentin  in  these  areas.  Into  the  spaces  of  the  granular  layer 
in  the  root  or  crown  portions  of  the  tooth  the  tubules  empty,  so 
to  speak,  and  in  some  instances  they  have  been  observed  to  pass 
beyond  for  some  distance  into  the  cementum  and  the  enamel. 
Practically  every  specimen  of  enamel  shows  that  here  and  there 
dentinal  tubules  penetrate  its  substance  for  a  clearly  perceptible 
distance,  a  condition  which  may  render  very  much  less  unreasona- 
ble the  observed  fact  that  occasionally  teeth  are  encountered 
where  enamel  responds  to  stimuli. 


b' 

c' 

■ 

f£'   y*  * 

,\suwHnaHH| 

4 

b  — 

>4 

KHbHBhj^H 

a 

Fig.  101. — Longitudinal  ground  section  of  tooth  showing  fields  of  dentin  at  a,  a'  and 
enamel  at  b,  b' .  ~  In  the  body  of  the  dentin  at  some  distance  from  the  dentoenamel 
junction  and  the  granular  layer  at  c,  c'  large  numbers  of  interglobular  spaces  are  seen 
at   d,  d' . 

The  granular  layer  of  Tomes  should  not  be  confused  with  the 
interglobular  spaces  (Figs.  100  and  101),  which  are  located  in  the 
body  of  the  dentin  at  some  distance  from  the  granular  layer. 
These  spaces  are  more  marked  in  the  crown  portion  of  the  dentin 
and  in  the  gingival  third  of  the  root,  and  are,  beyond  certain 
limits,  evidences  of  hypoplastic  phenomena  (imperfect  develop- 
ment) of  the  dentin  matrix  and  dentinal  tubnles.  They  are 
plainly  visible   in   ground   sections   with   a  high   or  low   power. 


ENAMEL,    DENTIN,    AND   CEMENTUM  233 

In  fresh  specimens  they  are  filled  with  calcified  or  semi-calcified 
dentin  matrix,  or  protoplasm.  A  few  tubules  may  pass  through 
the  space.  In  old  specimens  the  spaces  appear  dark,  being  filled 
with  debris  from  the  grinding  process.  They  have  been  called 
interglobular  spaces,  (i.  e.,  spaces  between  globules)  for  the  rea- 
son thai  similar  outlines  can  be  made  by  zones  of  spheres. 

Within  certain  limits  as  to  size  and  number,  the  interglobular 
spaces  may  be  considered  as  not  abnormal  characteristics  of  den- 
tin. Every  specimen  of  dentin,  however,  is,  strictly  speaking,  not 
a  normal  one  if  considered  from  the  standpoint  of  the  inter- 
globular spaces,  for  these  must  be  viewed  as  evidences  of  tem- 
porary arrestments  of  development. 

The  chemical  composition  of  dentin  may  be  outlined  as  fol- 
lows : 

Calcium   phosphate,  66% 

Calcium  carbonate,  3  to     4% 

Magnesium   phosphate,  1  to     2% 

Organic  matter,  27  to  28% 

100% 

Cementum 

It  is  that  bone-like  tissue  which  envelops  the  root  of  the  tooth  in 
its  entirety  and  which,  beginning  as  a  slender  covering  at  the 
enamel  line,  gradually  increases  in  thickness  until  the  apical  re- 
gion is  reached,  where  it  is  the  thickest.  The  cementum  is  de- 
veloped from  the  fibrous  envelope  of  the  tooth  follicle — the  so- 
called  follicular  wall.  It  differs  from  bone  in  that  it  does  not 
contain  any  Haversian  systems ;  in  that  it  possesses  no  blood  or 
nerve  supply  of  its  own,  but  depends  exclusively  for  its  nutrition 
and  innervation  upon  the  peridental  membrane;  and  in  that  from 
the  pathological  standpoint,  it  has  no  reparative  power,  except 
in  so  far  as  this  occurs  through  the  agency  of  the  peridental  mem- 
brane. The  cementum  is  deposited  in  layers,  the  deposition  of 
a  new  layer  not  beginning  until  the  previous  one  is  completely 
calcined.  These  layers,  or  lamellae,  are  distinguishable  under  low 
and  high  amplifications  and  represent  the  incremental  lines  of 
the  cementum  (Figs.  102  and  103).  Within  its  substances  are 
found  the  lacunae  or  spaces  containing  active  cells  from  the  follic- 
ular wall — the  ccmcntoblasts,  which  became  encapsulated  during 
the  calcification  process.     From  the  lacuna?  a  considerable  num.- 


234 


DENTAL    PATHOLOGY 


ber  of  small  canals  lead  out,  and  these  communicate  "with  similar 
small  canals  from  other  lacuna?.  These  small  canals  are  the 
canaliculi  and  they,  as  well  as  the  lacunce,  as  has  been  stated,  are  in 
healthy  eementum  filled  with  protoplasmic  matter  (Fig.  104). 

The  matrix  is  granular  in  some  locations  and  fibrous  in  others. 
In  decalcified  specimens  in  which  the  organic  portion  of  the  ee- 
mentum is  adherent  to  the  dentin,  the  fibrous  character  of  the  ma- 
trix is  plainly  visible  in  some  localities.    As  the  eementum  calcifies, 


r 


-fi  m 


Fig.  102. — Transverse  ground  section  at  the  apical  region  of  a  root.  In  the  apical 
region  and  in  root  bifurcations  and  trifurcations  the  eementum  is  the  thickest.  The 
lamellae  or  layers  of  eementum  may  here  be  seen  especially  at  a;  the  dentin  at  b;  and 
the  root  canal   at   c. 


through  the  agency  of  the  eementoblasts  in  the  peridental-mem- 
brane-to-be,  some  of  the  fibers  of  the  latter  tissue  in  its  em- 
bryonic stage  become  encased  in  the  eementum  (Fig.  105).  They 
are  to  be  found,  as  seen  in  Fig.  105,  not  in  proximity  to  the 
granular  layer,  but  at  some  distance  therefrom  in  eementum  rather 
younger  in  development.  The  similarity  in  development  between 
eementum  and  subperiosteal  bone  lends  credence  to  our  belief 
that  the  fibrous  appearance  of  the  eementum  matrix  is  due  to 


I  \  will..    DENTIN,     Wl>    CEMENTU  \l 


235 


the  deposition  of  inorganic  salts  in  a  fibrous  framework,  and 
als0  to  the  Pad  that  wherever  calcification  is  not  carried  on 
to  full  completion  the  semicalcified  libers  persisl  as  such.  These 
fibers  bear  to  cementum  the  same  relationship  in  genesis  as  Shar- 
pey's  fibers  do  to  bone. 

The  lacuna  of  variable  size  and  shape  are  practically  absenl 
in  the  thin  portion  of  the  cementum  (Figs.  106  and  107),  but  are  to 


Fig  103— Transverse  ground  section  of  tooth  at  the  beginning  of  apical  third  of 
root.  Observe  that  here  the  thickness  of  cementum  is  markedly  less  than  what  it  is 
farther  apically.      a,     a'   lamellae   of   cementum;    b,   dentin;    c,   root   canal. 

be  found  in  considerable  numbers  wherever  the  cementum  is 
thick  and  in  hypercementosis.  They  are  located  in  areas  nearer 
the  dentin,  as  shown  in  Fig.  108,  but  may  also  be  found  equidis- 
tant from  the  granular  layer  and  the  external  cementum  surface 
(Fig.  109).  The  lacuna?  are  particularly  abundant  in  the  apical 
region  and  in  the  bifurcations  and  trifurcations  of  molars  (Fig. 
110).  The  layers  of  cementum  next  to  the  peridental  membrane 
and  those  next  to  the  dentin  as  a  general  rule  contain  fewer 


236 


DENTAL    PATHOLOGY 


lacunas  than  those  in  the  central  portion.  In  hypercementozed 
specimens  the  lacunae  are  distributed  throughout  the  tissue  with- 
out  regard   to   form,    number,    or   arrangement.      The   tissue   is 


Fig.    104. — Thick   area   of   cementum   in   the   bifurcation   of   the   roots    of  a   molar,   showing 
lacuna"  and  canaliculi  and  intercommunication   of  canaliculi. 


characterized,  however,  by  the  presence  of  large  numbers  of 
lacunae.  The  form  and  size  of  the  lacunae  vary  within  certain 
limits    in    the    same    tooth,    and    the    canaliculi    branch    out    in 


ENAMEL,    DENTIN,    AND   CEMENTUM 


237 


c\<r\  direction,  although  principally  toward  the  peridental  mem- 
brane rather  than  toward  t be  denl in. 

DenliiKil  tubules  here  and  there  penetrate  into  the  cementum 
for  some  distance  and  anastomose  with  the  canaliculi  of  the 
lacunae.  It  is  a  difficull  matter,  however,  to  see  this  arrangement 
even  with  the  highest  power  of  the  microscope  in  all  cases,  but 
ilic  author  has  seen  it  in  a  sufficient  dumber  of  cases  to  warrant 
him  in  believing  that  such  is  the  ease,  and  that  if  it  can  not 
a  e  b' 


Fig.  105.— -Longitudinal  ground  section  showing  at  a  dentin,  at  b,  b'  clear,  glossy, 
so-called  hyaline  cementum  and  at  c,  a  more  recent  cementum  formation  than  at  b,  in 
which  intraalveolar  libers  of  the  peridental  membrane  appear  encapsulated  in  the  cementum 
and  at  d  some  few  lacuna;  with  their  respective  canaliculi.  At  c,  c'  the  granular  layer 
is  seen. 

be  demonstrated  in  all  cases  it  is  not  because  the  dentinal  tubules 
and  canaliculi  do  not  communicate,  but  rather  because  mi- 
croscopes are  not  sufficiently  powerful  to  demonstrate  it.  As 
to  whether  or  not  a  system  of  nutrition  is  thus  established 
to  the  cementum  from  the  dentin,  and  to  the  dentin  from  the 
cementum,  is  as  yet  an  unsolved  problem  in  dental  physiology. 
There  are  those  who  believe  that  such  is  the  case,  but  convincing 
proof  thereof  is  as  yet  lacking.7    R.  R.  Andrews  believes  that  in 


7Choquet:     Precis  D'Anatomie  Dentaire. 


Fig.  106. — Ground  section,  longitudinal,  showing  gingival  third  of  root.  The  cementum 
appears  devoid  of  lacuna;.  The  darker  lines  running  at  right  angles  with  the  tubuli  are 
artifacts — cracks  in  the  specimen  caused  by  shrinkage  in  drying,  filled  with  air  and  pow- 
dered tooth  substance  from  grinding. 


b  — 


Fig.    107. — Ground   section,   longitudinal,    showing   hyaline   cementum   devoid   of   lacuns 
and  canaliculi,  a,  a',  dentin;   b,  V ,  hyaline  cementum. 


i:\'a\ii:i.,   i>i:\ti.\,   and  ci;\ii:\ti   \i 
a  b 


289 


rf' 


a.. 


Fig.  10S. — Longitudinal  ground  section  of  cementum  showing  lacunae  in  areas  near 
dentin  at  a;  fibers  of  peridental  membrane  incased  in  the  cementum  at  b.  The  granu- 
lar  layer  is  seen  at   c;   the   width   of  cementum   is  from   d,  d' . 


I'ig.    109. — Longitudinal   ground   section   in   ginghal    third   showing  at   a,   lacunas   and   canal 
iculi    equidistant   from   granular   layer   at   b,    b' ,   and   external   cementum   surface   at    c. 


240 


DENTAL   PATHOLOGY 


the  fully  formed  cementum  the  processes  of  the  cementum  cor- 
puscles undoubtedly  anastomose  with  those  of  the  peridental 
membrane,  with  each  other,  and  with  the  processes  of  the  granu- 
lar layer  just  within  the  dentin.8 


Fig.    110. — The    cementum    in    the   apical    region    of   the   roots    of   an    upper    first   bicuspid. 
The  section  did  not  involve  the  root  canal.     The  dark  spots  represent  the  lacunae. 


The  chemical  composition  of  cementum  according  to  von  Bibra 
is  as  follows : 


Calcium  phosphate, 

48.73% 

Calcium    carbonate, 

7.22% 

Magnesium  phosphate, 

0.99% 

Soluble  salts, 

0.82% 

Organic  matter, 

42.24% 

100.00% 

If  this  analysis  is  compared  to  that  of  bone,  it  will  be  seen 
that  cementum  contains  18.90  per  cent  more  organic  matter  than 
bone,  and  8.94  per  cent  less  inorganic  matter. 

sAndrews,  R.  R.:     Calcification,  Dental  Cosmos,  January,   1912. 


CHAPTER  X 1 1 

DEVELOPMENT  OF  THE  TEETH 

From  the  fiftieth  to  the  sixtieth  day  of  intrauterine  life  the  first 
step  in  the  development  of  the  teeth  becomes  evident.  At  this  time 
a  thickening  of  the  stratum  malpighii  of  the  oral  epithelium  along 
the  peripheral  area  of  the  jaws  is  to  he  observed.  This  thickening 
of  the  oral  epithelium  progresses  in  the  direction  of  the  under- 
lying connective  tissue  and  constitutes  the  dental  hand  or  ridge 
(Figs.  Ill  and  112).  The  dental  groove,  a  term  frequently  en- 
countered in  connection  with  the  embryology  of  the  teeth,  can 
refer  only  to  the  appearance  of  a  transverse  vertical  section  of 
a  developing  jaw  where  it  will  be  seen  that  the  underlying  con- 
nective tissue  has  been  scooped  out,  so  to  speak,  the  groove  be- 
ing filled  with  masses  of  epithelial  cells — the  epithelial  band — a 
term  which  more  accurately  describes  the  early  stages  of  tooth 
embryology  than  the  term  dental  ridge.  If  we  picture,  as  sug- 
gested by  Magitot,1  a  rope  of  epithelial  cells  snugly  fitting  into 
a  depression  in  the  connective  tissue,  it  will  facilitate  a  correct 
conception  of  the  dental  hand  and  d ratal  groove,  the  band  being 
the  epithelial  rope  and  the  dental  groove  being  the  grooved  bed 
in  which  the  rope  rests.  The  dental  band  is  convex  externally 
and  concave  internally.  From  the  concave  surface,  about  mid- 
way between  the  apex  and  the  base  of  the  band,  an  epithelial  pro- 
jection— the  dental  lamina,— grows  out  lingually  almost  at  right 
angles  to  the  vertical  diameter  of  the  band.  This  projection  does 
not  occur  at  any  one  particular  locality,  but  extends  along  the 
entire  length  of  the  band.  A  shelf  growing  out  at  right  angles 
to  the  band  will  explain  better  the  relationship  of  the  dental 
lamina  to  the  dental  band. 

From  each  of  twelve  points  on  the  dental  lamina,  in  each  jaw, 
an  epithelial  cord  grows  out,  at  first  in  a  horizontal  direction  to- 


JLegros,   Ch.,   and   Magitot,   V..:     Dental   Follicle. 

241 


242 


DENTAL   PATHOLOGY 


ward  the  lingual  aspect  of  the  primitive  jaw,  and  then  in  a  di- 
rection almost  at  right  angles  from  the  lamina.  Of  these  cords, 
the  anterior  ten  are  destined  to  form  the  enamel  organs  of  the  de- 
ciduous teeth,  and  the  posterior  two,  those  of  the  permanent  first 
molars,  of  each  arch.     The  epithelial  cord  is  composed  of  epithe- 


^iaf^H 


Fig.  111. — First  evidence  of  tooth  development.  The  stratified  squamous  epithelium  is 
seen  dipping  into  the  subadjacent  connective  tissue  and  forming  the  dental  band  or  ridge. 
a,  epithelial  band  progressing  in  the  direction  of  the  underlying  connective  tissue;  b,  b' , 
and   b" ,    thickened   epithelial    layer;    c,    underlying   connective   tissue. 


DEVELOPMENT    OF    THE    TEETH 


243 


lial  cells  from  the  lamina,  and  the  latter,  in  turn,  from  the  periph- 
eral cells  of  the  dental  hand.  As  each  epithelial  cord,  which 
is  an  outgrowth  of  the  dental  lamina,  proceeds  downward  and 
somewhat  lingually,  and  after  obtaining  a  certain  length,  it  un- 
dergoes characteristic  changes  which  materialize  about  the  ninth 


\ 


J 


Fig.  112. — A  slightly  later  stage  than  in  the  preceding  illustration  showing  the  begin- 
ning of  the  invagination  of  the  epithelial  cord  which  will  result  in  the  formation  of  the 
four  layers  of  the  enamel  organ,  a,  epithelial  cells  from  the  more  superficial  or  older 
strata  of  the  Malpighian  layer;  b,  younger  strata  from  Malpighian  layer  from  which 
dipping  of  epithelium  occurs;  c.  epithelial  cord  beginning  to  undergo  the  invagination 
which  will  result  in  the  formation  of  the  four  distinct  groups  of  cells  of  the  enamel  or- 
gan;   d,   condensation   of   underlying  connective   tissue. 


244 


DENTAL   PATHOLOGY 


week  of  embryonal  life.     These  changes  result  in  the  eventual 
formation  of  the  enamel  organ. 

There  occurs  an  upward  invagination  in  the  case  of  the  lower 
enamel  organs,  and  a  downward  invagination  in  the  upper,  which 
progresses  until  a  hood-shaped  organ  has  resulted  which  sur- 
rounds a  condensation  of  connective  tissue  cells  (the  dentin-forming 
organ,  or  dental  papilla).     The  enamel  organ  as  now  constituted 


.•'vf&Vjiy! 


mi 


\ 


b 


Fig.  113. — The  four  sets  of  cells  of  the  enamel  organ;  a,  the  internal  or  the  layer  of 
the  ameloblasts;  b,  cells  of  the  stratum  intermedium;  c,  cells  of  the  stellate  reticulum, 
and  d,  of  the  external  layer.  Portions  of  the  follicular  sac  are  seen  at  c,  surrounding 
the  dental  papilla  and  enamel  organ;  from  the  follicular  wall  the  cementum  and  alveolar 
process   will   develop. 


will  consist  of  an  external  layer  of  epithelial  cells;  of  an  internal 
layer,  which  is  formed  from  the  invagination  of  the  outer  layer  of 
the  enamel  hud;  of  a  layer  of  cells  in  close  contact  with  the  inner 
aspect  of  the  internal  layer — the  stratum  intermedium;  and  of 
a  number  of  stellate  cells  occupying  the  space  between  the  external 
and  internal  layers — the  stellate  reticulum  (Fig.  113).  The  stra- 
tum intermedium  and  the  stellate  reticulum  originate  from  the 
inner  cells  of  the  dental  lamina,  and  these  in  turn  from  the  inner 


DEVELOPMENT   OF    THE    TEETH  245 

cells  of  the  dental  band.  The  internal  Layer  consists  of  the 
enamel  building  cells  ameloblasts,  or  enameloblasts ;  the  external 
Layer  begins  to  show  signs  of  an  atrophic  process  prior  to  the 
completion  of  the  enamel;  and  the  cells  of  the  stratum  inter- 
medium and  those  of  the  stellate  reticulum  are  probably  concerned 
in  supplying  the  ameloblasts  with  such  nutritional  elements  as 
are  required  by  them  during  enamel  formation.  In  other  words, 
and  to  present  a  mental  sketch  of  the  germ,  the  enamel  or- 
gan is  a  double  hood  containing  between  the  external  hood  and 
the  internal  hood  the  cells  of  the  stratum  intermedium  and  stel- 
late reticulum,  the  double  hood  enclosing  a  specialized  mass  of 
embryonal  connective  tissue  cells — the  dental  papilla,  or  dentin- 
forming  organ.  For  a  time  the  enamel  organ  remains  connected 
to  the  dental  lamina  by  means  of  a  slender  corcl  of  epithelial  cells 
designated  as  the  epithelial  cord.  It  gradually  atrophies,  and  by 
the  time  the  thirteenth  week  of  embryonal  life  has  been  reached, 
the  cord  is  ruptured  and  the  tooth  follicle  proceeds  in  its  de- 
velopmental work  independent  of  any  connection  with  the  oral 
epithelium. 

The  enamel  organ  of  all  the  deciduous  teeth  may  be  said  to  ap- 
pear about  the  eighth  week  of  embryonic  life;  the  dental  papilla 
about  the  ninth  week ;  the  follicular  wall  which  encircles  the 
tooth  follicle,  (i.  e.,  enamel  organ  and  dental  papilla),  rises  from 
the  base  of  the  dental  papilla  and  appears  at  the  tenth  week; 
the  follicle  closure  and  simultaneous  rupture  of  the  cord  occurs 
about  the  thirteenth  week;  and  the  formation  of  dentin  begins 
about  the  sixteenth  week.2 

The  enamel  buds  of  the  permanent  teeth,  with  the  exception  of 
tin  first,  second  and-  third  molars,  begin  to  develop  about  the 
sixteenth  week  from  the  epithelial  cord  of  the  corresponding 
temporary  tooth,  the  process  of  development  being  analogous  to 
that  of  the  temporary  teeth.  The  first  molars  develop  from  in- 
dependent invaginations  of  the  dental  ridge  about  the  fifteenth 
week  of  intrauterine  life  in  exactly  the  same  way  as  do  the  de- 
ciduous teeth  (see  above)  ;  the  second  molars  develop  from  an 
offshoot  of  the  epithelial  cord  of  the  first  molar,  about  the  third 


:Legros,    Ch  ,    and   Magitot,    E. :      Chronology   of   the    Dental    Follicle   in    Man.      Trans- 
lation by  M.   S.   Dean. 


246  DENTAL   PATHOLOGY 

month   after  birth ;  and  the  third  molars  develop  from  offshoots 
of  the  second  molar,  about  the  second  or  third  year  after  birth. 

The  calcification  of  the  enamel  proceeds  from  within  outwards, 
while  that  of  the  dentin  from  without  inwards.  A  divergence  of 
opinion  exists  in  regard  to  the  process  by  which  enamel  is  cal- 
cified, particularly  so  concerning  the  ultimate  fate  of  the  cells 
of  the  enamel  organ.  Aside  from  the  facts  that  the  internal 
epithelial  layer  of  the  enamel  organ  is  the  enamel-building  layer ; 
that  the  cells  of  the  stratum  intermedium  are  probably  substitu- 
tion enamel  cells  (i.e.,  they  replace  functionally  exhausted  amelo- 
blasts)  ;  and  that  the  cells  of  the  stellate  reticulum  are  the  agen- 
cies of  nourishment  to  the  active  enamel-building  cells — nothing 
based  upon  actual  observations  has  so  far  been  brought  out  that 
could  be  considered  otherwise  than  as  mere  theories.  The  amelo- 
blasts  are  elongated  cells  which  become  more  or  less  hexagonal 
by  mutual  apposition.3  They  are  in  close  relation  to  the  large 
round  cells  of  the  stratum  intermedium.  The  cells  of  the  stellate 
reticulum  are  connected  among  themselves  by  means  of  processes, 
a  reticulated  appearance  being  the  result.  The  cells  of  the  ex- 
ternal layer,  after  the  cells  of  the  stellate  reticulum  have  atro- 
phied, coalesce  with  those  of  the  internal  layer  and  persist  for 
some  time  after  the  eruption  of  the  teeth  as  Nasmyth  's  membrane. 
The  enamel  begins  to  form  on  the  deciduous  teeth  about  the  seven- 
teenth week  of  embryonic  life,  ending  about  the  sixth  month  after 
birth.  On  the  permanent  teeth  it  begins  to  form  at  birth  or 
slightly  before  birth,  and  ends  about  the  twelfth  year  on  the  crown 
of  the  third  molar.4 

Dentin 

As  has  been  previously  noted,  the  dental  papilla,  or  dentin- form- 
ing organ,  makes  its  appearance  about  the  ninth  week,  or  ap- 
proximately a  few  days  after  the  beginning  of  the  formation  of 
the  dental  groove  by  the  inward  growth  of  the  dental  band. 
The  dental  papilla  ( dentin-f orming  organ,  dental  bulb)  is  a  mass 
of  embryonal  connective-tissue  cells  (Fig.  114),  whose  peripheral 
cells  assume  a  quasicolumnar  shape  and  arrange  themselves  in 
a  fairly   regular   way.     The   cells   have   a   well-defined  nucleus 


3Tomes:      Dental  Anatomv,    Philadelphia,   P.   Blakiston's   Son   &   Co. 
4Andrews,    R.    R.:      Dental    Cosmos,    1912. 


MA  ELOPMENT   OF    THE   TEETB 


247 


occupying  a  position  in  the  interna]  third  of  the  cell  toward  the 

denial  papilla,  and  differ  in  appearance  as  to  whether  dentin  is 
being  actively  produced  or  not.  During  active  dentinification 
the  ends  of  the  odontoblasts  next  the  already  formed  dentin  are 


Fig.  114. — Same  stage  of  development  as  seen  in  the  preceding  illustration.  The  fol- 
licular sac  which  springs  from  the  base  of  the  dental  papilla  is  seen  surrounding  the  de- 
veloping  organ,      a,    follicular   wall;    b,    dental    papilla;    c,    internal    or    ameloblastic    layer. 

expanded;  at  periods  of  arrested  dentinification  the  cells  seem 
longer  and  their  ends  more  slender  and  rounded.  The  process 
of  calcification  of  dentin   (dentinification)   which  precedes  that 


248 


DENTAL   PATHOLOGY 


of  enamel  calcification  (amelification)  by  a  few  days  advances 
from  without  inwards,  the  odontoblasts  probably  discharging  the 
calcific  material  so  as  to  envelop  the  protoplasmic  process  with 
which  each  odontoblast  is  provided  at  its  external  end.  As  cal- 
cification proceeds,  a  gradual  recession  of  the  odontoblasts  oc- 
curs, and  simultaneously  with  this  there  is  an  elongation  of  their 
external  protoplasmic  processes  which,  occupying  the  lumen  of 
the  tubes  thus  formed,  become  the  dentinal  fibers,  or  fibrilhc,  or 
fibers  of  Tomes. 

It  is  not  at  all  improbable  that  the  intt  rt  nbular  substance  (den- 
tin  matrix)    is   the  result   of  the   calcification   of   cells   from   the 


nths  after  birth 


40th  week  (birthl 
30th  week  embryo 
18th  week  embryo 
17th  week  embryo 


Fig.    115. — Calcification    of   the    deciduous   teeth.      (Peirce.) 


Fig.    116. — Calcification   of   the   permanent   teeth.      (Teirce.) 

dental  papilla,  this  process  being  likewise  presided  over  by  the 
odontoblasts. 

Cementum  and  Peridental  Membrane 

As  will  be  remembered,  about  the  tenth  week  of  embryonic  life 
there  are  seen  to  grow  out  from  the  base  of  each  dental  papilla 
certain  cells  which  become  the  fibrous  envelope  of  the  tooth  germ 
(follicular  wall)  (Fig.  114).  This  closes  simultaneously  with  the 
severance  of  the  cord  about  the  thirteenth  week.  This  fibrous 
layer  has  a  dual  function:  the  cells  of  the  outer  layer  are  con- 


DEVELOPMENT   OP    THE    TE]   ill  2  l!» 

eerned  in  the  building  up  of  the  osseous  structure  of  the  alveolar 
process,  those  of  the  inner  layer  being  concerned  in  the  building 
of  cementum.  It  should  be  added  here,  however,  thai  a  line  of 
demarcation  between  the  externa]  and  internal  layer  is  prac- 
tically  an  impossibility.  At  the  time  of  eruption  of  t he  teeth 
through  the  gums  there  still  remain  portions  of  the  tooth  root, 
cementum,  and  alveolar  process  to  develop.  The  alveolar  proc- 
ess is  produced  simultaneously  with  the  cementum  in  order  to 
provide  for  the  means  of  retention  of  the  tooth  in  the  jaw.  The 
process  of  root  development  is  best  studied  from  the  diagrams 
(Figs.  115  and  116). 


CHAPTER  XIII 

HYPOPLASIA,  MICROSCOPIC  AND  MACROSCOPIC 

In  the  discussion  of  hypoplasia  in  its  microscopic  and  macro- 
scopic aspects  we  aim  to  describe  abnormalities  of  the  teeth  in 
structure,  size,  form  and  number.  The  term  atrophy  will  not  be 
used  for  the  reason  that  in  its  general  acceptance  it  conveys  the 
thought  of  retrograde  changes  after  an  organ  has  attained  its  full 
growth,  atrophy  being  defined  as  the  series  of  changes  taking 
place  in  a  fully  formed  organ  leading  to  a  loss  of  weight,  size 
and  function  consequent  upon  such  causes  as  overuse,  disuse, 
excessive  pressure,  faulty  diet,  and  nutritional  and  trophic  dis- 
turbances.   Excess  of  waste  over  assimilation  leads  to  atrophy. 

The  teeth,  barring  pathologic  conditions  and  the  physiologic 
wearing  away  of  their  occlusal  surfaces,  remain  unchanged 
throughout  the  life  of  the  individual.  They  are  not  subject  to 
retrogressive  changes  through  overuse  or  lack  of  use,  (exclud- 
ing, of  course,  the  manifestations  of  these  conditions  upon  the 
peridental  membrane,  which  is  not,  strictly  speaking,  an  integral 
part  of  the  tooth,  but  accessory  thereto),  and  neither  are  the  hard 
tissues  improved  in  quality,  to  much  of  an  extent,1  after  they 
have  become  calcified.  Enamel  and  dentin  have  no  power  of 
repair.  AVe  exclude  from  this  consideration  such  calcifications 
as  take  place  in  the  dentinal  tubules  as  a  normal  process  with 
advancing  age,  or  as  the  result  of  pathologic  influences.  Also 
are  excluded  increases  in  the  thickness  of  eementum  of  a  strictly 
pathologic  character,  and  the  increases  of  eementum  in  certain 
areas,  or  the  resorptions  in  others  which  take  place  continuously 
until  such  time  as  the  entire  complement  of  teeth  has  erupted 
and  the  occlusion  for  the  given  individual  has  become  perma- 
nently established.  All  changes  in  the  eementum,  constructive 
or  destructive  in  character,  are  governed,  as  will  be  studied  later 
in  the  text,  by  either  functional  changes  in  the  peridental  mem- 
brane or  by  the  influence  of  osteoclastic  (cementoclastic)  cells. 


1See   discussion  of  enamel  on  page  226. 

250 


BYPOPLASIA.    MICROSCOPIC    A.ND    MACROSCOPIC 


251 


As  the  size,  form,  and  structure — the  latter  up  to  certain  limits — 
of  the  crowns  of  teeth  appear  after  their  eruption,  so  will  they 
remain  unaltered  through  life,  except,  of  course,  as  the  result  of 
disease  processes. 

DENTAL  HYPOPLASIA 

Enamel,  Dentin,  and  Cementum 

Imperfect  or  insufficient  development  of  a  part  resulting  from 
abnormal  influences  during-  intrauterine  life,  or  during  develop- 


Fig.  117. — Hypoplastic  defects  of  the  enamel.  Incomplete  calcification  of  the  fissures 
and  faulty  development  of  the  ena.mel  rods  in  the  area  of  a  cusp,  a,  incomplete  fusion 
of  the  cusps  of  a  bicuspid  resulting  in  a  defecting  calcified  fissure;  b.  disturbance  in  the 
arrangement  of  the  enamel  rods.  The  histological  characters  of  the  enamel  rods  in  the 
area  at  b,  are  wanting. 

mental  periods  after  birth,  is  classified  as  hypoplasia.  Under  this 
heading  the  study  of  developmental  defects  of  the  enamel,  den- 
tin, and  cementum  will  be  undertaken. 

Etiology. — By  hypoplasia  of  the  teeth  is  meant  incomplete,  de- 
fective or  misdirected  development  of  the  tissues  of  the  teeth. 
These   developmental  faults   may  be   only  microscopic,   or  both 


252 


DENTAL    PATHOLOGY 


microscopic  and  macroscopic  in  character,  and  are  dependent  for 
their  production  upon  unbalanced  nutritional  processes  affect- 
ing the  dental  follicle  at  any  time  from  the  beginning  of  its  for- 
mation to  the  completed  development  of  the  tooth,  which  is 
marked   by   the   calcification    of   the   apical    portion   of   the   root 


Fig.    IIS. — Hypoplastic    defect    of    the    enamel.    Int  ision    of    the    cusps 

molar  producing  a  defective  fissure  as  shown  at  c.  Areas  of  normal  enamel  at  a,  a' : 
a  small  area  of  normal  dentin  at  b. 

and  the  establishment  of  the  apical  foramen  as  it  will  persist  with 
whatever  changes  may  occur  in  its  diameter  throughout  the  life 
of  the  tooth.  The  inorganic  salts  which  enter  into  the  formation 
of  the  enamel  are  not  carried  to  the  enamel  organ  in  sufficient 
amounts  as  the  result  of  faulty  metabolism  or  of  a  diet  poor  in 
inorganic  salts.    Again,  it  may  result  from  a  defective  combination 


EYPOPLASIA,    MICROSCOPIC    AND    MACROSCOPIC  253 

between  the  inorganic  salts  and  the  albuminous  binding  sub- 
stance. 

The  periods  of  nutritional  insufficiency  may  be  due  to  path- 
ologic conditions  in  the  mother  which  will  affecl  the  deciduous 
teeth,  directly,  or  in  the  advanced  stages  of  development  by  hav- 
ing induced  in  the  infanl  changes  affecting  its  physiological  ac- 
tivities. It  is  well  to  remember  in  this  connection  that  the  be- 
ginning of  calcification  of  these  teeth  is  included  in  the  period 
from  the  sixteenth  to  the  twentieth  week  of  intrauterine  life. 
Disturbances  in  the  mother  interfering  with  the  nutritional  proc- 
esses in  the  fetus  may.  in  some  instances,  affect  the  first  per- 
manent molar,  as  the  calcification  of  ibis  tooth  is  known  to  begin 
in  some  cases  one  or  two  months  before  birth.  The  transmission 
from  mother  to  fetus  of  certain  systemic  intoxications,  particu- 
larly syphilis,  may  result  in  hypoplasia  of  certain  teetli  whose 
calcification  does  not  begin  until  after  birth.  Concerning  con- 
ditions after  birth,  it  can  be  stated  that  any  disease  or  deviation 
from  the  normal  in  the  child  may  result  in  temporary  arrests 
of  calcification  of  the  enamel  and  dentin,  or  in  defective  calci- 
fication; but  particularly  important  are  the  exanthematous  fevers 
— measles,  chicken  pox.  scarlet  fever,  smallpox,  etc. — which  may 
leave  a  hypoplastic  impression  upon  the  enamel  and  dentin.  A 
rise  in  temperature  of  whatever  origin,  if  it  persists  for  as  little 
as  a  few  days,  may  leave  its  permanent  impress  upon  the  teeth. 
Infectious  processes  in  the  roots  of  the  deciduous  teeth  may  cause 
changes  in  the  underlying  permanent  tooth  sac:  resulting  in  de- 
fective calcification.2 

Developmental  defects  of  enamel  affect  certain  areas  of  as 
many  teeth  as  are  in  process  of  development  at  the  time  the  nu- 
tritional errors  were  taking  place.  It  is  in  this  way  that,  knowing 
the  chronology  of  tooth  development,  and  in  particular  that  of 
calcification  of  the  enamel,  it  is  a  comparatively  easy  matter  to 
ascertain  the  period  in  the  life  of  the  embryo  or  after  birth 
when  these  disturbances  of  nutrition  occurred. 

Histologically  these  defects  in  the  enamel  are  due  to  insuffi- 
ciency in  the  number  of  enamel  rods,  imperfect  calcification  of 
the  rods,  and  likewise  to  deviations  in  the  quantity  or  quality  or 


•Turner,    T.    S.:      Transactions    Odontological    Society   of   Great    Britain,    XXXVJT,    in 
Bennett's  Dental  Surgery. 


254 


DENTAL   PATHOLOGY 


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BYPOPLASIA,    MICROSCOPIC    AND    MACROSCOPIC 


255 


both  of  the  cementing  substance  (Figs.  117,  118,  11!),  and  120). 
Two  interesting  specimens  of  marked  enamel  hypoplasia  are 
shown  in  Pigs.  11!'  and  120.  As  previously  stated,  the  histologic 
defect  may  be  so  intense  as  to  give  rise  to  a  macroscopic  defect 
visible  on  the  external  enamel  surface,  such  being  the  case  with 
the  specimen  under  consideration.  In  Fig.  120  a  disturbance  in 
the  disposition  of  the  enamel  rods  has  occurred.  The  rods,  in- 
stead of  following  the  perpendicular  direction  to  the  surface,  as 


-b' 


Fig.  119. — Hypoplasia  of  the  enamel  producing  an  external  macroscopic  defect  on  the 
labial  surface  of  an  incisor.  At  o  is  observed  the  area  of  disturbed  enamel  rod  calci- 
fication; the  enamel  rods  that  are  present  are  of  a  low  grade  of  calcification  and  stunted 
in  their  growth  and  the  interprismatic  substance  is  not  present  in  sufficient  amounts. 
Normal  enamel  is  seen  at  b  and  b' :  normal  dentin  at  c  and  c' ,  and  defects  in  the  calci- 
fication  of  the  dentin  in  the   form   of   interglobular  spaces   at   d. 


is  the  case  in  approximal  surfaces,  appear  wavy  and  very  irregu- 
lar in  their  course  and  faulty  in  their  calcification.  The  more 
marked  cases  show  a  deficiency  or  absence  of  enamel,  and  the 
surface  of  the  tooth  is  irregular  and  rough.3     (Fig.  119.) 

Cases  of  complete  or  partial  absence  of  enamel  are  also  occa- 
sionally encountered.     This  form  of  exaggerated  enamel  hypo- 


3Bennett:      Dental   Surgery,    New   York,   Win.    Wood   &   Co. 


256 


DENTAL    PATHOLOGY 


plasia  is  designated  under  the  term  of  enamel  agenesia  (Fig. 
121).  Systemic  disturbances  of  a  severe  type  undoubtedly  occur 
at  the  calcification  period  of  the  affected  teeth. 

In  the  dentin,  hypoplastic  defects  arc  represented  by  imperfect 
tubular  formation,  incomplete  tubular  calcification,  and  defects  in 
the  dentin  matrix  (Fig.  122). 

These  hypoplastic  changes  are  manifested  in  the  shape  of  an 
increase  in  the  size  and  number  of  the  interglobular  spaces.     These 


Fig.  120. — Hypoplasia  of  the  enamel  in  the  approximal  surface  of  an  incisor.  At 
a.  a'  enamel  rods  which  do  not  follow  the  direction  of  normal  enamel  rods  in  these  loca- 
tions are  seen.  Also  the  abrupt  decrease  in  the  thickness  of  the  enamel,  from  left  to 
right  of  the  picture  should  be  observed. 


spaces  are  found  in  the  dentin  throughout  the  entire  extent  of  the 
tooth,  but  are  more  prominent  near  the  enamel.  They  represent 
stages  of  arrested  activity  of  the  odontoblastic  layer.  Any  patho- 
logic influence  strong  enough  to  produce  hypoplasia  of  the  enamel 
will  likewise  produce  arrested  calcification  in  certain  areas  of  the 
dentin.  The  formation  of  tubules  will  come  to  a  standstill,  and 
upon  the  recovery  of  the  formative  organ  the  formation  of  tubules 
will  begin  at  some  distance  from  the  point  where  growth  had 
stopped.     The  sections  of  organic  matrix  which  undergo  partial 


BYPOPLASIA,    MICROSCOPIC    AND    MACROSCOPIC 


257 


Fig.    121. — A    case    of    enamel    agenesia.      All    the    deciduous    teeth    are    affected.      The 
dentin  is  nowhere  protected  by  enamel  and  is  of  a  yellowish  color  typical   of  dentin   when 
-    1  to  the   fluids  of  the  mouth  and  to  extraneous  substances. 


m'...-d 


V    ;M 


Fig.  122. — Decalcified  section  showing  a  multitude  of  interglobular  spaces.  These 
are  areas  of  incomplete  develoDment  and  calcification  of  the  dentin  matrix  and  dentinal 
tubuli.  a,  cementum  (hyaline);  b,  normal  dentin;  c,d,e,f,  interglobular  spaces  of 
Czermak. 


258  DENTAL    PATHOLOGY 

calcification,  or  do  not  undergo  any  calcification  at  all,  constitute 
the  interglobular  spaces  first  described  by  Czermak  after  whom 
they  are  named  the  interglobular  spaces  of  Czermak. 

Examples  of  hypoplasia  of  the  deciduous  teeth  are  rare:  when 
it  occurs  it  is  located  high  in  the  crowns  toward  the  gingival  mar- 
gin, the  occlusal  surfaces  being  almost  invariably  normal.  The 
reason  for  this  lies  in  the  fact  that  the  period  of  greatest  suscepti- 
bility to  abnormal  influences  in  utero,  so  far  as  the  teeth  are  con- 
cerned, is  during  the  last  month  or  two  of  intrauterine  life,  and 
reaches  to  the  beginning  of  the  second  year  after  birth.  On  the 
other  hand,  hypoplasia  of  the  permanent  teeth  is  relatively  frequent 
in  some  teeth,  while  others  are  rarely  affected ;  e.g.,  the  bicuspids 
and  second  molars  are  seldom  the  seat  of  hypoplasia,  while  the  third 
molars  upper  and  lower  are  frequently  the  seat  of  defective 
development  affecting  the  crown  or  roots  of  the  tooth,  or  both,  and 
is  in  practically  all  instances  the  result  of  obstructions  in  the  path 
of  their  eruption. 

Pathologic  Anatomy. — In  the  study  of  structural  hypoplasia  of 
the  enamel  or  dentin  any  deviation  from  the  appearance  of  mi- 
croscopic sections  which  are  within  the  limits  of  normality  is  to 
be  considered  as  a  developmental  (hypoplastic)  defect.  By  this 
we  mean  that  the  enamel  should  have  a  uniform  appearance,  and 
the  rods  under  high  magnification  should  show  the  transverse 
markings  indicative  of  the  method  of  individual  rod  formation 
(Figs.  88  and  89).  In  the  case  of  the  enamel,  the  lack  of  cement- 
ing substance  produces  the  white  spots  so  frequently  encoun- 
tered, also  spots  from  the  faintest  to  the  deepest  shade  of  brown. 
Two  cases  of  extensive  enamel  hypoplasia  are  reported  by  the 
late  Dr.  G.  V.  Black4  in  which  a  general  absence  of  cementing 
substance  was  responsible  for  an  enamel  which  was  white,  chalky, 
and  easily  disintegrated.  In  these  places  the  enamel  is  so  easily 
disturbed  or  penetrated  by  means  of  a  cutting  instrument  that  an 
explorer,  after  the  surface  has  been  penetrated,  will  in  some  ex- 
aggerated cases  convey  a  sense  of  chalkiness.  These  white  spots 
may  or  may  not  affect  the  entire  thickness  of  enamel.  Patho- 
logically these  are  significant  defects  because  of  their  offering 
favorable  areas  for  the  rapid  spread  of  caries.  Imperfect  enamel 
calcification  is  frequently  encountered  in  the  fissures  of  molars  and 


4Black,  G.   V.:     Operative   Dentistry,   i. 


HYPOPLASIA,    MICROSCOPIC    AND    MACROSCOPU 


259 


Fig.   123. 

Fig.  123. — Hypoplasia  of  the 
enamel  in  the  shape  of  a  slight 
reddish    brown    discoloration. 


Fig.   124. 

Fig.    124. — Hypoplasia   of   the  enamel   in   the   shape 
of    intense    reddish    brown    discoloration. 


Fig.    125. — A  case  of  brown   stain  affecting  the  enamel   on  the  labial   surfaces  of  the  central 
and  lateral   incisors  only. 


bicuspids,  and  in  the  lingual  pit  of  the  upper  central  and  lateral 
incisors,  when  the  pit  is  present;  in  the  linguogingival  ridge  of 
the  upper  cuspid,  when  fissured  or  grooved ;  in  the  buccal  groove 
of  the  upper  first  molar.  In  these  locations  the  defect  is  due 
to  incomplete  closure  of  the  fissure. 


260 


DENTAL    PATHOLOGY 


Fig.     126. — A    slight    hypoplasia    of    the 
enamel    on    the    labial   surface   of   an    upper 

cuspid. 


Fig.    1  -27. — Hypoplasia  of  the   enamel   on 
the    labial    surface    of    an    upper    cuspid. 


Fig";    128. — Hypoplasia  of  the  enamel  on  the  Fig.    129. — Hypoplasia  of  the  enamel 

labial    surfaces    of    upper    left    and    upper    right     in    an    upper    left    central    incisor.      The 
lateral     incisors,     semilunar     in     shape.  enamel     is     tr'ansversed     by     horizontal 

and     vertical     depressions     of     a     brown 

Ci  ill  il'. 


The  formation  of  rods  has  been  insufficient  to  produce  a  smooth 
bridging  over  or  closure  of  the  fissure.  A  large  number  of  sec- 
tions which  have  been  examined  in  the  course  of  our  studies  show 
frequently  the  presence  of  calcified  amorphous  bodies  in  these 
defective  fissures.     In  the  milder  forms  of  hypoplasia  the  bands 


HYPOPLASIA,    MICROSCOPIC    AND    MACROSCOPIC 


261 


of  Retzius  appear  larger  and  are  of  a  deeper  brown  color  than  is 
the  case  in  normal  specimens,  testifying  to  a  lack  of  uniform  cal- 
cification of  the  rods  in  their  long  diameter.    The  enamel  being 


Fig.    130. — Hypoplasia   of   the   enamel    in  Fig.   131. — Hypoplasia  in  the  crown  of  a 

an   upper   right   lateral   incisor.  lower     molar.        The     enamel      is     studded 

everywhere    with    soft    chalky    spots    (chalky- 
enamel ). 


Fig.  132. — Hypoplasia 
of  the  crown  of  an  upper 
molar.  The  enamel,  as  in 
the  previous  picture,  con- 
tains a  large  number  of 
chalkv     areas. 


Fig.  133. — Hypoplasia  of  the  enamel  in  upper  rcclars.  The 
extent  of  the  faulty  development  is  shown  externally  by  an 
extreme  irregularity  of  surface  upon  the  occlusal  and  approx- 
imal    aspects    of    the    teeth. 


deposited  in  segments  represented  by  the  bands  of  Ketzius.  it 
stands  to  reason  that  any  disturbance  which  will  affect  the  proc- 
ess of  enamel  formation  will  be  represented  by  variations  from 


262  DENTAL   PATHOLOGY 

the  normal  throughout  the  segment  of  enamel  in  the  course  of 
deposition.  Inasmuch  as  insufficient  or  imperfect  enamel  forma- 
tion is  the  result  of  a  temporary  arrest  of  activity  throughout 
the  extent  of  the  ameloblastic  layer,  it  consequently  follows  that 
all  enamel  that  would  have  been  formed,  in  the  absence  of  disturb- 


Fig.    134. — Hypoplasia  of  Ihe   enamel   in   lower   molars.     The   occlusal   and   approximal    sur- 
faces, as  in  previous  specimen   are   extremely   irregular. 


Fig.    135. — Hypoplasia   of   the   enamel   in  Fig.    136. — Hypoplasia   of   the   enamel    in 

an  upper  cuspid.  Several  faint  lines  run-  an  upper  central.  The  band  in  the  cen- 
ning  horizontally  across  the  enamel  mar  ter  of  the  crown  is  the  dividing  line  he- 
the   appearance   of  the   crown.  tween   two   periods   of  hypoplasia   which   oc- 

curred at  different  times.  The  incisal 
third,  the  gingival  third,  and  the  "band" 
are   the   normal   enamel   areas   of  the   tooth. 

ing  factors,  is  affected.  While  this  view  is  upheld  by  a  number  of 
pathologic  investigators,  instances  have  come  under  our  own  ob- 
servation in  which  the  defective  formation  has  not  followed  a 
segment  or  band  of  Retzius  in  its  entirety,  but  has  manifested  it- 


HYPOPLASIA,    MICROSCOPIC    AND    MACROSCOPIC  263 

self  in  the  shape  of  a  relative  preponderance  of  cementing  sub- 
stance throughout  the  depth  of  several  segments  in  the  direction 
of  the  enamel  rods.    The  greater  amount  of  cementing  substance 

at  the  sacrifice  of  the  number  of  enamel  rods  is  characterized 
microscopically  by  dark,  cloudy  areas  surrounded  by  enamel  rods 
of  normal  appearance.  This  increase  in  the  depth  of  color  is  be- 
lieved to  be  due  to  tin1  presence  of  actual  pigment.8 

Developmental  defects  in  the  enamel  and  dentin,  when  pro- 
nounced, give  rise  to  conspicuous  malformations  of  the  crown 
which  may  range  from  the  slightest  brownish  discoloration,  as 
seen  in  Fig.  123,  to  most  marked  broien  spots  in  the  enamel  as 
seen  in  Pigs.  124  and  125,  and  from  the  faintest  chalky  whiteness 
in  the  enamel,  as  seen  in  Fig.  126,  to  as  pronounced  a  hypoplasia  as 
seen  in  Figs.  127  to  134.  Again,  from  a  faint  line  or  lines  in  the 
enamel  (Fig.  135)  sufficiently  pronounced  to  mar  its  appearance  to 
as  wide  a  banel  as  that  shown  in  Fig.  136.  In  other  cases  several 
grooves  may  be  present  in  the  labial  side  of  the  crown,  and  in  still 
others  the  hypoplastic  defects  assume  a  rough  granular  or  pitted 
appearance — the  granular  elefect  of  the  enamel. 

The  pit  form  of  enamel  defect  consists  of  either  one  single  pit 
surrounded  by  healthy  enamel  structure,  or  of  a  series  of  pits ; 
the  former  may  be  located  anywhere  on  the  enamel  surface,  the 
latter  in  the  lower  half  of  the  crown  near  the  incisal  edge  in  the 
case  of  the  incisors  or  cuspids  or  near  the  occlusal  surface  in  the 
ease  of  the  bicuspids  or  molars.  The  more  pronounced  develop- 
mental defects  will  be  discussed  under  the  heading  of  macroscopic 
deformities  of  the  teeth  in  the  following  chapter. 


5Xoyes:     Dental   Histology  and   Embryology,   Philadelphia,   I.ca   &   Febiger. 


CHAPTER  XIV 

MACROSCOPIC  DEFORMITIES  OF  THE  TEETH 

Macroscopic  deviations  from  the  normal  may  affect  the  crown, 
the  root,  and  botli  the  crown  and  the  root  of  one  tooth,  of  several 
teeth,  or  of  all  the  teeth  in  the  same  month.  These  macroscopic 
deviations  may  be  so  slight  as  to  require  careful  examination  in 
order  to  detect  them.  In  these  cases  the  external  appearance  of 
the  tooth  is  slightly  affected  and  the  physiologic  function  not  at 
all.  In  other  instances  the  deviation  from  the  normal  is  so  ex- 
tensive as  to  mar  the  appearance  of  the  toolh  to  the  point  of  ren- 
dering its  identification  difficult  and  its  physiologic  function  incom- 
plete. Gross  deviations  in  size  may  affect  one  or  more  teeth,  or  all 
of  the  teeth  in  both  arches.  It  is  not  unusual  to  find  that  one  tooth 
is  larger  or  smaller  in  relation  to  the  other  units  of  the  same  arch, 
and  again  that  all  the  teeth  in  both  arches  are  either  too  small  or  too 
large  in  relation  to  the  size  of  the  mouth  and  to  facial  contour. 
The  upper  central  incisors  and  canines,  the  lower  second  bicuspid 
and  the  third  molars,  upper  and  lower,  are  frequently  out  of 
harmony  with  their  fellows  in  the  arch.  Other  types  of  abnor- 
malities in  size  consist  in  a  disproportion  in  the  size  of  the  crown 
and  root,  as  is  seen  in  the  case  of  central  incisors  with  abnor- 
mally short  roots  and  upper  cuspids  with  abnormally  long  or 
short  roots.  Under  a  different  heading  will  be  studied  those  ab- 
normalities affecting  the  number  of  teeth  in  the  arch,  i.e.,  the 
presence  of  supernumerary  teeth,  and  the  congenital  absence  of 
one  or  more  units  from  the  dental  arch. 

Abnormalities  of  Form  Affecting  the  Crowns  and  Roots  of  the 

Permanent  Teeth 

Central  Incisors. — The  most  important  macroscopic  defects  in 
the  central  incisors  are  those  which  affect  the  cervicolingual 
ridge.  This  ridge  may  be  either  insufficiently  developed  or  over- 
developed to  such  an  extent  as  to  result  in  the  presence  of  a  pseudo- 
cusp  (Figs.  137  and  138).    The  division  of  the  cervicolingual  ridge 

264 


\l  \(  ROSCOPIC    DEFORMITIES    OF    THE    TEETH  265 

by  ;i  nearly  central  fissure,  as  seen  in  some  instances,  results  in  the 
presence  <>f  two  cervicolingual  ridges— a  mesiolingual  ;m<l  <i  disto- 
lingnal    ridge.3      (Fig.   139.)      In    Pig.    140  a    reproduction    of   a 


Fig.    137. — Overdeveloped   cervicolingual  Fig.    139. — Fissured  cervicolingual   ridge 

ridge  in  upper  left  lateral  incisor.  in    lateral    incisor. 


Fig.    138.  —  Hypoplasia   of   the   cervicolingual    ridge    of   u]>]>er   incisors. 

ground  see  ion  of  an  incisor  with  an  overdeveloped  cervicolingual 
ridge  simulating  a  cusp,  is  seen.  An  extra  root  arising  from  the 
lingual  aspect  is  another  abnormality  that  may  affect  this  tooth. 


'Bennett:      Dental   Surgery,   New    York,   Win.   Wood   &   Co. 


266 


DENTAL   PATHOLOGY 


A  disproportion  between  the  size  of  a  crown  and  its  root  may 
exist.  The  central  incisors  may  be  the  seat  of  severe  hypoplasia. 
(Figs.  141,  142,  and  143.)  The  root  only  may  be  imperfectly 
developed  (Fig.  144).  A  ground  section  shows  normal  microscopic 
characteristics,  notwithstanding  the  macroscopic  root  deformity 


Fig.  140.— Photomicrograph  of  a  central  incisor  with  an  overdeveloped  cervicolingual 
ridge  simulating  a  cusp,  a,  dentin;  b,  enamel;  c,  hypoplastic  defect  of  the  enamel  in  the 
under  surface  of  the  cervicolingual  ridge. 


(Fig.  145).    A  hypoplastic  defect  of  the  middle  lobe  of  the  central 
incisor,  the  so-called  Hutchinson's  notch,  is  shown  in  Fig.  146. 

The  upper  central  incisors  are  in  some  instances  much  larger 
in  size  in  proportion  to  their  neighbors.     When  present,  this  ab- 


MACROSCOPIC    DEFORMITIES   OF    THE    TEETH  207 

normality  in  size  generally  affects  both,2  the  right  and  left  cen- 
tral incisors. 

Upper  central  incisors  willi  abnormally  short  roots  are  some- 
times encountered. 


Fig.     141. — Severe    hypoplasia    of    upper  Fig.    142. — Severe  form   of  hypoplasia  in 

central    incisor,    embodying   the    microscopic         upper     incisor,     embodying    the    microscopic 
and  macroscopic  forms.  and    macroscopic    forms. 


Fig.   143.— Severe  form  of  hypoplasia  in  Fig.   144.— Hypoplasia  of  the  root  of  an 

upper     incisor     involving     the     crown     and         upper   incisor. 
the   root. 

The  lower  central  incisors  arc  rarely  the  seat  of  abnormalities. 
Lateral  Incisors. — The  upper  lateral  incisors  may  be  the  seat 


-P.urchard     and     Inglis:        Dental     Pathology     and     Therapeutics,     Philadelphia,     I.ea     & 
Febiger. 


268  DENTAL   PATHOLOGY 

of  macroscopic  defects  of  the  same  character  as  found  in  the 
central  incisors,  i.  e.,  underdevelopment  or  overdevelopment  of 
the  eervicolingual  ridge  and  the  presence  of  an  additional  root. 
The  lower  lateral  incisors  art1  rarely  the  seat  of  abnormalities. 
The  upper  lateral  incisor  is  frequently  the  seat  of  marked  macro- 
scopic aberrations,  the  crown  assuming  various  shapes,  in  addi- 


ng.   145. — Ground   section   of  specimen   shown   in    Fig.    144.      It   shows   normal   microscopic 
characteristics,    notwithstanding  the  gross   root   deformity. 

tion  to  a  disproportion  between  the  size  of  the  crown  and  that 
of  the  root.  A  peg-shaped  lateral  is  occasionally  encountered 
(Fig-.  147).  The  root  of  the  upper  lateral  incisor  may  he  de- 
flected labially,  as  seen  in  Fig.  14S.  Upper  lateral  incisors  are 
sometimes  found  with  abnormally  deep  eervicolingual  ridges  and 
a   median   fissure   two-thirds   across   their   vertical   diameters,      A 


MACROSCOPIC    DEFORMITIES    OP    THE    TEETH 


269 


lower  lateral   incisor  with   a    prong-like   process  on   the  lingual 

Mii-fact'  is  seen  in  Pig.  149. 

The  lower  lateral  may  have  two  roots  and  two  root  en  mils  i  Fig, 
L50).     The  two  roots  may  he  well   formed  and   independent  of  one 


Fig.     146. — Hypoplasia     of     the     incisal  Fig.    147. — Peg-shaped    upper    lateral    in- 

third    of    an    upper    incisor.       A    so-called  cisor.      As    the    length    of    the    picture    is 

Hutchinson's    tooth.       The    middle     lobe    is  twice  the  actual  length   of  the  tooth  it  does 

incompletely     developed     upon     the     incisal  not    convey    a    clear    idea    of    the    diminu- 

aspect.  tiveness    of    the    tooth. 


Fig.  148. — An  upper  right  lateral  in- 
cisor mesial  view  with  a  labial  deflec- 
tion  of  its   root. 


Fig.    '49 — A   prong-like   process   on   the   lin- 
gual   surface   of   the    lower    lateral    incisor    at    a. 


another,   or  the  deformity  may   consist   of  the   bifurcation   of   its 
normal  root  at  the  apical  third. 

Cuspids. — With  the  exception  of  a  disproportion  in  the  size 
of  this  tooth  as  com] tared  with  the  other  teeth  in  the  same  arch. 
the  cuspid  is  rarely  the  seat  of  macroscopic  defects,  although 


270 


DENTAL    PATH' 


rdevelopment  of  the  cervicolingual  ridge  may  be  encountered, 

and  in  some  instances  it   i^  so  marked  as  to  simulate  a  lingual 

Two  ere  hypoplasia  of  the  crown  of  an  upper 

id  are  seen  in  Figs.  151  and  152. 

A  series  of  short-rooted  upper  cuspids  is  shown  in  Fig.  153.    A 

series  of  long-rooted  upper  cuspids  is  shown  in  Fig.  lo4.     The 

deflection,  if  there  is  any.  of  the  root  of  the  upper  cuspid  is  as  a 


Fig.   150.  Fig.  151.  Fig.   :  rj. 

Fig.  150. — Lower  lateral  incisor,  with  two  roots. 

Fig.  151. — Severe  hypoplasia  of  upper  cuspid.     (Microscopic  and  macroscopic  defects.) 

Fig.  152. — A  marked  case  of  enamel  and  dentin  hypoplasia  ("microscopic  and  macro- 
scopic defects)  in  upper  right  cuspid  the  result  of  an  exanthematous  fever  from  which 
the  patient  suffered  at  the  time  at  which  the  tooth  was  being  calcified.  The  defect  and 
incomplete  development  has  affected  both  the  enamel  and  dentin. 


general  rule  in  a  distal  direction     Fig.  155  .  but  it  may  be  in  a 
mesial  direction,  as  shown  in  Fig.  156. 

TIih  occurrence  of  two-rooted  lower  cuspids  is  not  rare.    S 
mens  of  this  type  of  malformation  are  shown  in  Figs.  157  and 

158.     The  lower  cuspid  may  have  an  abnormally  short  root.     A 
supernumerary  root  in  a  lower  cuspid  occasionally  occurs  (Fig. 

159).    A  severe  hypoplasia  of  a  lower  cuspid  is  seen  in  Fig.  160. 


MACROSCOPIC    DEFORMITIES   OP   TEK    TEETH  271 

Bicuspids. — The  upper  first  bicuspid  may  have  a  crown  with 
three  cusps  and  a  trifurcated  root  as  shown  in  Figs.  161  and  162; 
also,  instead  of  the  usual  bifurcated  root  it  may  have  a  single  root 
with  two  canals  and  two  apical  foramina,  or  one  root  with  one  sin- 
gle canal  constricted  mesiodistally.  In  the  upper  second  bicuspid, 
when  the  root  is  bifurcated,  the  two  branches  may  be  united  by  a 


Fig.   153. — A  series  of  upper  cuspids  with  unusually  short   roots. 


Fig.    154. — A    series    of   upper   cuspids    with    abnormally    long   roots. 

band  of  cementum  for  some  distance  from  the  bifurcation  to  the 
apices  of  the  roots,  as  shown  in  Fig.  163.  The  lingual  root  of  the 
upper  first  bicuspid  may  be  deflected  to  the  extent  shown  in  Fig. 
164.  The  root  of  the  upper  second  bicuspid  may  be  abnormally 
small  and  stubby,  dividing  into  two  branches  in  the  apical  region, 
as  shown  in  Fig.  165.    In  the  case  of  three-rooted  upper  bicuspids 


272 


DENTAL    PATHOLOGY 


Fig.     155. — Distal    deflection    of    an    ni> 
per   right  cuspid. 


Fig.     156. — A    marked    deflection    to    the 
mesial    in    an    upper    right    cuspid. 


Fig.    157. — Lower  cuspids   with  two  roots. 


MACROSCOPIC    DKFOKMITIES    OF    THE    TEETB 


273 


Fig.   158.     Radiogram  of  a  lower  righl   cuspid  with  two  roots 


Fig.    159. — Supernumer  Fig.     160.— Marked    hy- 

ary    root    in    lower    cuspid.        poplasia  of  the  crown   ot   a 
lower  cuspid. 


Fig.     161. — Upper     first 
bicuspid     with     three     mots. 


Fig.    162. — Upper    right               Fig.       163.— An      upper             Fig.      164.— An  upper 

first     bicuspid     with     three         second    bicuspid    with    a   bi-        first    bicuspid    with  marked 

roots.                                                     furcated   root.                                  deflection     of     the  lingua! 

root. 


271 


DENTAL   I'A'l  HOLOGY 


the  disposition  of  the  roots  may  assume  either  one  of  two  relation- 
ships: (a)  there  may  be  presenl  a  mesiobu<-r;il,  ;i  distobuccal  and 
a  lingual  rool  (Fig.  161)  ;  or  (b)  one  rool  may  be  on  the  buccal  as- 
pect and  the  other  two  on  the  lingual  asju-ei  of  the  tooth,  as  shown 
in  Pig.  166.  There  may  exisl  a  disproportion  between  the  crown 
of  the  npper  first  bicuspid  and  its  root.  as  shown  in  Pig.  167.    A 


Pig     165.      Bifurcation    of    ,:  Pig.      166.     An      upper     bicuspid     witli 

an  up  bicuspid.  is  placed  buccally  and 

two  lingually. 


Fig.  167. — An  upper 
lirM  Bicuspid  with  an  ab- 
normally   long    root. 


Pig.    168.     A    hypoplaa 
tic  upper   bicuspid. 


Fig.      1 69.     Proi 
d(  fli  ction  '  of  an 

upper  bicuspid. 


hypoplastic  upper  bicuspid,  probably  the  first,  is  seen  in  Pig.  168, 
and  in  Pig.  169  a  view  of  an  upper  bicuspid  with  a  marked  deflee- 
i ion  of  the  root. 

The  upper  second  bicuspid  may  presenl  variations  affecting  the 
Dumber  and  size  of  its  roots.  As  a  general  rule  this  tooth  has  bu1 
one  root  and  our  canal,  the  latter  having  its  longest  diameter  in  a 
buccolingual  direction.     Deviation  from  this  type  may  consist  in 


MACKosconc    DEFORMITIES    OF    THE    TEETH 


275 


Fig.       170.     Upper      left 

e< I     bicuspid  ;     dispropor 

lion  between   the  size   "i    the 
crown   and   that    of   the   root 


I  ■"  i  k  •  171. — An  upper 
second  bicuspid  with  a 
dispi  oportionately  small 
root. 


Pig.  172.— A  lower 
first  bicuspid  with  two 
roots. 


Fig,     173. — Lower     sec- 
ond     bicuspid      with      two 

roots.        The     lingual     root 
is     partly     hidden     behind 

the    buccal. 


Fig.    17  l.  — A   lower  first 
bicuspid  w  ith  a  mai  ked  de 

flection  of  its  roots. 


Fig.  175.— Distal  deflec- 
tion of  the  root  of  the 
lower  righl  first  bicuspid. 


276 


DENTAL   PATHOLOGY 


Fig.  176. —  Disproportion  between  the 
size  of  the  crowns  and  roots  of  lower 
second  bicuspids.  Also  deflection  of  the 
roots  rendering  practically  impossible  the 
proper  treatment  and  filling  of  the  root 
canal. 


Fig.    177. — Hooked   root   in   lower 
bicuspid. 


Fig:  178. — Disproportion  be' 
the  crown  and  root  of  a  lower 
second   bicuspid. 


ween  Pig.     179.  —  Disproportion    between    the    sizr 

right        of   t lie   crown   and   that   of   the    root  and   deflec- 
tions   of    the    root    of    lower    first    bicuspids. 


MACROSCOPIC    DEFORMITIES   or    THE    TEETH 


277 


the  presence  of  two  or  three  foots,  each  with  its  respective  rod  ca- 
nal. Disproportion  between  the  size  of  the  crOwn  and  thai  of  the 
toot   of  the  upper  second  bicuspid  is  seen  ill  Pigs.   170  and    171. 

The   lower  first    bicuspid  may   have  a    lingual    cusp    larger   or 
smaller  than  the  average  type  of  lingual  cusp  for  this  tooth.    The 


Fig.     ISO. — Hypoplasia     of     the     lingual 
cusp    of    a    Inner    first    bicuspid. 


Pig.      1S1 

licuspid. 


-A    hypoplastic    tower    second 


Fig.    182. — Lower    left    second    bicuspid    with    six    cusps.      Lingual    and    occlusal    views, 
simulating  an  abnormal   lower   third.     A,   buccal   aspect;   D,   occlusal  aspect. 

lingual  cusp  of  the  lower  first  bicuspid  is  even  in  normal  speci- 
mens markedly  smaller  than  the  buccal  cusp,  but  in  some  abnormal 
specimens  it  is  nothing  more  than  a  rudimentary  cusp.  The  lin- 
gual surface  of  the  crown  may  be  free  from  fissures,  or  the  lin- 
gual cusp  may  be  bordered  on  the  mesial  and  distal  by  a  fissure 
which,  beginning  near  the  mesial  and  distal  marginal  ridges, 
reaches  over  onto  the  lingual  surface.    Also,  first  and  second  lower 


278 


DENTAL   PATHOLOGY 


bicuspids  with  two  roots  and  tivo  distinct  root  canals  are  occasion- 
ally found.  A  lower  first  bicuspid  with  two  roots  is  a  rare  ab- 
normality  (Fig.  172).     A  lower  right  second  bicuspid  with  two 


Fig.   1  S3. — The  roots  of  an  upper  molar  Fig.    184. — An   upper  second   molar  with 

united    by    bands   of    cementum.  its    three    roots    fused    together    by    means 

of  cementum. 


Fig.    185. — Upper    left   third    molar   with  Fig.     186. — An    upper    first    molar    with 

badly     deflected,     fused     and     hypercemen-         hooked   roots, 
tosed   roots. 


roots  is  seen  in  Fig.  171?.  In  these  cases  the  roots  may  be  fused  for 
a  section  of  their  length  by  means  of  a  band  of  cementum  or 
throughout  the  length  of  the  roots.     A  marked  deflection  of  the 


MACROSCOPIC    PEFOKMITIKS    OP    Till',    'III   II I 


279 


root  of  tlif  lower  firsl  bicuspid  is  sometimes  found,  as  shown  in 
Fig.  174.  The  deflection  in  this  case  was  toward  the  lingual.  A 
distal  deflection  of  the  root  of  the  lower  first  bicuspid  is  seen  in 
Pig.  175.  A  disproportion  between  the  size  of  the  crown  and  that 
of  the  root  of  the  lower  second  bicuspid,  and  a  deflection  of  the 
root.is  seen  in  Pig.  176.  A  hooked  root  in  a  lower  bicuspid  ren- 
dering impossible  successful  root  canal  treatment  and  filling  is 
shown  in  Fig.  177. 

Disproportion  betwet  n  tht  si:e  of  the  crown  and  that  of  the  root 
is  not  an  infrequent  occurrence  in  the  case  of  the  lower  bicuspids. 
The  root  is  proportionately  either  considerably  longer  or  shorter 


Fig.    187. — Deflection   to   buccal   ami   dis- 
tal   roots    of    upper    first    molar. 


Fig.     188. — A     supernumerary     root 
upper   molar. 


than  the  crown,  or  vice  versa  (Figs.  178  and  179).  The  dispropor- 
tionately long  root  may  be  either  deflected,  or  hypercementosed,  or 
both.  These  root  deflections  and  the  fact  that  the  abnormally  long 
root  not  infrequently  has  a  very  slender  termination,  render  diffi- 
cult, if  not  impossible,  the  treatment  and  filling  of  the  root  canal. 
Hypercementosis  of  the  abnormally  long  root  of  a  lower  first  bi- 
cuspid is  not  an  uncommon  phenomenon. 

The  lower  second  bicuspid  may  present  a  disproportion  between 
the  crowm  and  the  root.  The  root  may  be  either  too  short  or  too 
long.  The  root  may  be  extremely  deflected,  usually  to  the  left. 
Figs.  180,  181,  and  182  are  reproductions  of  hypoplastic  lower 
bicuspids. 


280 


DENTAL    PATHOLOGY 


First  Molars. — A  not  infrequent  macroscopic  abnormality  in 
the  upper  first  molars  is  the  presence  of  a  cusp  between  the  mesial 
and  lingua]  cusps  in  the  gingival  margin.    An  elevation  in  some 


Fig.    1X9. — T.ower   right   first   molar   with 
Supernumerary    root    on    the   lingual    aspect. 


Fig.  190. — Supernumerary  root  on  disto- 
buccal    aspect    of    a    lower    first    molar. 


Fig.   191.— A   lower   firsl 

molar  with  a  supernumer- 
ary root  between  the  me- 
sial and  distal  roots  on  the 
lingual  aspect. 


Fig.  192. — A  lower 
first  molar  with  three 
roots.  The  supernumer- 
ary springs  from  the  dis- 
tal   root. 


Fig.  193. — A  lower  first 
molar  with  three  roots;  su- 
pernumerary root  on  inci- 
sal   aspect. 


portion  of  the  occlusal  surface  simulating  an  additional  cusp  is 
another  form  of  abnormality  found  in  this  tooth.  The  roots  of  the 
first  molar  are  generally  well  developed  and  independent  of  one 
another.     There  is,  however,  in  some  cases,  a  fusion  of  the  two 


MACROSCOPIC    DEFORMITIES    OF    THE    TEETH 


lis] 


buccal  roots,  or  of  one  buccal  root  with  the  lingual  root,  or  of 
the  three  roots,  the  Latter  being  a  rare  occurrence.  These  fusions 
are  due  to  a  growth  of  cementum  between  the  roots  (Figs.  183, 
1*4,  and  185).  The  roots  of  the  upper  firsl  and  second  molars 
may  be  markedly  deflected  and  hooked  !  Figs.  186  and  187)-.  A 
diminutive  supernumerary  root  may  be  presenl  on  an  upper  molar 
Pig.  188). 

The  lower  first  molar  is  sometimes  minus  the  distal  buccal  cusp. 
Tomes  found  this  cusp  absent  in  18  per  cent  of  a  series  of  skulls 
examined  by  him.4 

The  abnormalities  of  this  tooth  consist  in  the  presence  of  a  super- 


Fig.   194. — Four  well-developed  roots 
in  lower  left  second  molar. 


Fig.    195. — A   hypoplastic   lower  third 
molar. 


numerary  root  in  relation  with  the  distal  root  (Fig.  189).  This 
extra  root  is  usually  located  on  the  lingual  aspect  of  the  tooth, 
but  may  be  also  found  on  the  buccal  aspect  of  the  tooth  (Fig. 
190).  In  Fig.  191  is  seen  a  lower  first  molar  with  an  extra  root  be- 
tween the  mesial  and  distal  roots  on  the  lingual  aspect.  A  lower 
first  molar  with  a  bifurcated  distal  root  is  seen  in  Fig.  192.  A 
lower  first  molar  with  a  supernumerary  root  in  relation  to  the 
mesial  root  is  seen  in  Fig.  193. 

Second  Molars. — The  upper  second  molar  may  be  a  three-  in- 
stead of  a  four-cusped  tooth,  in  which   case  the  crown  is  of  a 


■•Bennett:      Loc  cit 


282 


DENTAL    PATHOLOGY 


quasitriangular  shape,  and  the  roots  are  completely  fused  by 
means  of  cementum.  The  three  roots  of  this  tooth  are  frequently 
subject  to  abnormal  variations.     The  lower  second  molar  is,  how- 


Fig-.    196. — Dwarfed   upper  third   molar. 


Fig.    197. — Dwarfed   lower  third   molars. 


Fig.    198. — Dwarfed    upper   third   molar. 


ever,  less  frequently  the  seat  of  abnormal  development  than  the 
first  molar.  The  roots  may  converge  at  their  apices.5  A  lower 
second  molar  may  present  four  well-developed  roots  (Fig.  194). 


BBarrett :      Loc.  cit. 


MACROSCOPIC    PKFOKMITIKN    OF    THE    TEETH 


\is:\ 


Third  Molars.— -The  third  molar  is  frequently  the  scat  of  ab- 
normal development.  Prom  Ihe  almosl  perfect  upper  and  lower 
third  molars  closely  resembling  their  respective  second  molars, 
every  type  of  deviation  is  found,  even  down  to  the  dwarfed  molar. 


Fig.     199. — Hypoplastic     upper     third 
molars. 


Fig.    200. — Marked    deviation    of    the 
roots  of  an  upper  third   molar. 


Fig.    201.  —  Upper   third    molars   with   double   deflection    of   the   buccal    roots   and   single    de- 
flection  of   the   lingual   roots. 

The  lower  third  molar  may  present  a  fairly  well-developed  crown 
having  three  short  roots  fused  together,  as  shown  in  Fig.  195.  It  may 
also  present  a  supernumerary  root  located  between  the  mesial 
and  the  distal  roots.     The  upper  and  lower  third  molars  may  he 


284  DENTAL   PATHOLOGY 

as  insufficiently  developed  as  shown  in  Figs.  196,  197,  and  198.  In 
Figs.  199  and  200  are  shown  upper  third  molars  with  marked 
developmental  deviations.  An  upper  third  molar  with  double 
deflection  of  the  buccal  roots  is  shown  at  Fig.  201. 

The  upper  third  molars  may  exhibit  roots  so  badly  curved  as  to 
render  any  attempt  at  root  canal  treatment  absolutely  impossible. 
A  supernumerary  root  may  be  present,  springing  from  the  base 
of  the  lingual  root. 

Lower  third  molars  are,  as  a  rule,  possessed  of  roots  which  are 
deflected  distally  to  various  extents.  The  mesial  and  distal  roots 
may  be  single  deflected  cones,  terminating  in  a  very  slender  tip, 
or  the  distal  root  may  be  a  single  deflected  cone  and  the  mesial 
root  bifurcated — an  incomplete  fusion  of  the  mesiobuccal  and 
mesiolingual  roots.  The  mesial  and  distal  roots  may  be  fused 
into  one  single  cone  in  which  the  lines  of  fusion  make  it  possible 
to  segregate  them.  The  fusion  in  such  cases  may  be  complete  or 
only  partial,  a  space  being  present  between  the  bifurcation  and 
the  beginning  of  fusion.  "When  the  two  roots  are  fused,  the 
joined  apices  may  or  may  not  be  deflected  to  the  distal.  Oc- 
casionally a  lower  third  molar  is  encountered  with  two  roots 
which,  bifurcating  near  the  apex,  give  the  tooth  the  appearance 
of  having  four  roots.  The  mesial  root,  whether  bifurcated  or 
not,  may  be  proportionately  much  shorter  than  the  distal  root. 
A  rootlet  may  occasionally  be  found  between  the  two  roots  upon 
their  lingual  aspect. 

Geminated  Teeth 

By  geminated  teeth  is  meant  the  fusion  of  two  or  more  teeth 
by  means  of  enamel  or  cementum.  During  the  developmental 
period  it  is  probable  that  distortion  by  pressure  of  the  enamel 
organs  of  the  fused  teeth  takes  place,  and  again,  this  distortion 
or  misplacement  may  affect  the  developing  roots  only,  in  which 
case  the  crowns  will  lie  separated  from  one  another,  but  the 
roots  will  be  fused  or  united  by  means  of  cementum.  The  fusion 
or  gemination  of  teeth  may  affect  either  the  deciduous  or  the 
permanent  teeth.  Fig.  202  shows  two  deciduous  incisors  erupted 
with  their  roots  fused  to  one  another  by  means  of  cementum.    Fig. 


.MACKosconc    ltKFOKMlTIES   OF    THE    TEETH 


285 


203  shows  an  upper  central  and  Lateral  incisor  erupted  fused  to 
one  another  \'<>v  a  distance  of  aboul  one-third  the  length  of  their 
roots  from  their  apices  to  an  imaginary  line  of  junction  between 
the  apical   third  and   gingival  two-thirds.     In  Pig.  204  a  molar 


Fig.     202. — Geminated 
deciduous    incisors. 


Fig.  203. — Geminated  up- 
per central  and  lateral  inci- 
sors. 


Fig.    204. — Geminated    molar   and 
bicuspid;    possibly    two    bicuspids. 


Fig.       205. — Geminated 
and   third   molars. 


upper      seconi 


and  bicuspid,  possibly  two  bicuspids,  are  shown,  the  crowns  and 
one  half  of  the  roots  being  fused  together.  In  Figs.  205,  206, 
and  207  upper  second  and  third  molars  are  shown  fused  to  one 
another  in  their  roots. 

Distortions  and  displacements  of  portions  of  the  enamel  organ 


286 


DENTAL   PATHOLOGY 


result  occasionally  in  the  presence  of  enamel  tissue  in  abnormal 
locations.  In  Fig.  208  is  seen  a  rounded  mass  of  enamel  tissue 
{enamel  pearl)   in  a  concavity  on  the  lingual  root  of  an  upper 


Fig.      206. — Geminated      upper 
second  and   third   molars. 


Fig.     207. — Geminated    upper    second    and    third 
molars. 


Fig.  208. — Enamel  pearl  on  upper 
left  second  molar  located  in  the 
concavity  on  the  lingual  root  which 
shows  a  tendency  toward  bifurca- 
tion. 


209. — Enamel  pearl  in   upper 
right   first  molar. 


left  second  molar,  and  in  Fig.  209  is  seen  an  enamel  pearl  in  an 
upper  right  molar  at  the  neck  of  the  tooth. 


CHAPTER  XV 
ABNORMALITIES  IN  THE  NUMBER  OF  TEETH 

Supernumerary  Teeth 

Abnormalities  of  number  in  excess,  i.  e.,  supernumerary  teeth, 
are  encountered  more  frequently  than  abnormalities  due  to  the 
absence  of  teeth.     A  supernumerary   tooth  may  be  of  abnormal 


Fig.    J 10. — A  peg-shaped  supernumerary  tooth   between  the   upper  central  incisors. 


Fig.    211. — Two    tuberculated    supernumerary    incisors    in    the    same   arch. 

form  or  may  have  a  normal  appearance,  usually  that  of  one  of 
its  immediate  neighbors.     A  supernumerary  peg-shaped  tooth  is 

287 


288 


DENTAL   PATHOLOGY 


Fig.    212. — A    tuberculated    supernumerary   tooth    between    the    incisors.      The    left    central 
incisor   is    not    shown    in    this   view    as    it    was    located    lingually. 


Fig.   213. — A   peg-shaped  supernumerary  tooth  located  lingually   to  the   upper   incisors. 


Fig.    214. — A    supernumerary    central    in    perfect    alignment    between    normal    incisors. 


si   PERN1    MERAR1    TEETH 


2K!J 


at  limes  round  between  the  two  een.1  ral  incisors,  causing  a  very  un- 
sightly malformation  (Fig.  210).  One  or  two  supernumerary  tu- 
berculated  incisors  may  be  present  in  the  same  arch  (Figs.  211  and 


Fig.    215. — A    supernumerary    upper    incisor    fused   to    the    normal    central    incisor. 


Fig.    216. — Supernumerary    molar    between    the    upper    second    anil    third    molars. 


Fig.    217. — A    fourth    molar   in   place. 


212).  A  peg-shaped  supernumerary  tooth  may  be  located  imme- 
diately behind  one  of  the  normal  incisors,  the  latter  being  forced  out 
of  normal  alignment  (Fig.  213).    The  supernumerary  incisor  may 


290  DENTAL   PATHOLOGY 

also  be  of  normal  form ;  Fig.  214  shows  a  case  in  which  five  in- 
cisors were  present,  each  tooth  having  attained  practically  normal 
development.  A  supernumerary  upper  right  lateral  incisor  of 
normal  form  may  be  located  lingually  from  the  central  incisors. 
A  supernumerary  incisor  may  erupt  fused  to  either  one  of  the 
normal  incisors  (Fig.  215).  In  the  molar  region  a  reversion  of 
type,  as  exemplified  by  the  presence  of  a  fourth  molar  on  both 
sides  of  each  arch,  is  not  infrequently  observed.  The  supernu- 
merary molar  may  be  smaller  in  relation  to  its  fellows,  but  still  of 
somewhat  regular  form  (Fig.  216).  In  Fig.  217  is  shown  a  super- 
numerary molar  (fourth  molar)  occupying  a  position  distal  to 
the  third  molar.  A  unicuspid  tooth  is  sometimes  found  occupy- 
ing a  position  between  the  first  and  second  molars  on  the  buccal 
side. 


CHAPTER  XVI 
ABNORMALITIES  IX  THE  NUMBER  OF  TEETH 

Absence  of  Teeth 

Etiology. — The  absence  of  teeth  from  the  arch  may  be  due  to 
the  noneruption  of  fully  calcified  teeth;  to  nonevolution  of  the 
tooth  germ;  to  the  failure  of  calcification  processes  in  the  dental 
follicle;  to  injury  to  the  developing  tooth  germ  from  traumatism  or 
infectious  processes:  to  the  accidental  removal  of  the  permanent 
tooth  germ  by  the  extraction  of  the  deciduous  tooth;  to  the  trans- 
formation of  the  tooth  germ  into  an  odontoma.1 

Whenever  a  calcified  tooth  does  not  erupt,  it  is  a  case  of  in- 
carceration or  impaction  according  as  to  whether  the  path  lead- 
ing to  normal  position  in  the  arch  is  free  or  obstructed.  This  ab- 
normality affects  the  third  molars,  upper  and  lower,  the  upper 
second  bicuspids,  the  upper  laterals  and  upper  and  lower  cuspids 
with  greater  frequency  than  other  teeth.  Incarceration  of  a 
permanent  tooth  is  sometimes  associated  with  the  retention  of 
the  corresponding  deciduous  tooth  until  later  in  life  than  normal, 
and  occasionally  even  throughout  the  life  of  the  individual  (Figs. 
218  and  219).  The  influence  of  heredity  in  these  abnormalities 
of  number  is  veil  shown  in  the  case  of  the  upper  laterals',  this 
tooth  bein<j-  sometimes  absent  through  several  generations,  in  one 
or  several  members  of  the  same  family. 

R.  M.  Capon2  has  reported  on  the  mouths  of  a  whole  family, 
parents  and  seven  children,  the  youngest  twelve  years  of  aire 
and  the  eldest  twenty-seven,  from  which  no  less  than  twenty- 
seven  of  the  permanent  teeth  missing  had  never  erupted.  The 
mouths  of  the  three  girls  showed  a  deficiency  of  eight  teeth.  The 
eldest  of  the  three  had  never  erupted  the  upper  lateral  incisors 
and  two  of  the  lower  bicuspids.  The  other  two  girls  have  some 
of  the   bicuspid   teeth   missing.      One  of  the   girls   at   the   age   of 


'Bennett:      Dental   Surgery. 
-Capon,    R.    M.:      Dental   Record. 


291 


292 


DENTAL   PATHOLOGY 


sixteen  retained  the  temporary  laterals.  The  hoys,  four  in  num- 
ber, have  between  them  a  deficiency  of  eighteen  teeth.  The  father 
had  never  erupted  the  upper  lateral  incisor,  and  the  mother  is 
the  only  member  of  the  family  in  whom  all  the  teeth  have 
erupted. 

While  the  absence  of  the  complete  dentition,  both  deciduous 
and  permanent,  and  of  the  permanent  alone,  is  an  extremely  rare 
occurrence,  nevertheless  eases  of  this  kind  are  on  record  in  den- 
tal literature.  Bennett  reports  a  case  in  which  the  upper  cuspids 
occupying  positions  near  the  median  line,  one  upper  molar  on 
each  side,  and  one  lower  molar,  also  on  each  side,  were  the  only 
teeth  of  the  permanent  set  to  erupt.  An  insufficiency  in  the  num- 
ber of  teeth  is  less  frequently  encountered  than  an  excess  (super- 


Fig.  218. — Deciduous  upper  second  mo- 
lar retained  until  late  in  life,  occupying 
the  position  of  the  upper  second  bicuspid 
which   never   developed. 


Fig.  219. — A  retained  lower  left  second 
deciduous  molar.  The  tooth  follicle  of  the 
second   bicuspid   evidently   never  developed. 


numerary  teeth).  In  one  extreme  case  the  deciduous  upper  cen- 
tral and  lateral  incisors  on  the  left  side,  and  the  deciduous 
central  incisor  on  the  right  side,  had  been  shed,  and  up  to  the 
age  of  nine  years  there  was  no  indication  that  their  permanent 
successors  would  erupt,  the  space  between  the  right  lateral  in- 
cisor and  left  cuspid  being  occupied  by  one  peg-shaped  tooth. 

The  absence  of  the  permanent  upper  right  lateral  incisor  is  a 
rather  frequent  abnormality.  A  case  of  this  kind  is  shown  in 
Fig.  220.  The  absence  of  a  lower  incisor  is  a  rare  abnormality. 
A  lower  bicuspid  may  be  absent  and  when  it  fails  to  erupt  it  is 
the  second  more  frequently  than  the  first  (Fig.  219).  The  per- 
manent first  molar  mav  be  absent  owing  to  the  failure  of  the  fully 


ABNORMALITIES    IN    THE    NUMBER   OK    TEETH 


293 


calcified  tooth  to  erupt,  its  presence  in  the  substance  of  the  jaw 
being  made  evident  with  the  aid  of  radiography.  A  case  of  this 
kind  which  gave  rise  to  systemic  complications,  is  shown  in  Fig. 
221.     The  absence  of  the  permanent  cuspids  is  rarely  the  result 


Fig.    220. — Absence   of   the    upper    right    lateral    incisor. 


Fig.  221. — Noneruption  of  permanent  tower  first  molar. 


294 


DENTAL   PATHOLOGY 


of  the  nondevelopment  of  the  tooth,  but  in  most  instances  is  due 
to  the  failure  of  the  fully  formed  tooth  to  erupt  (Figs.  222  and 
223).  The  absence  of  deciduous  teeth  is  occasionally  ob- 
served. In  extreme  cases  perhaps  only  the  deciduous  cuspids 
and  second  molars  will  erupt.  In  other  instances  the  lower  de- 
ciduous incisors  may  be  absent.  We  recently  saw  a  case  of  absence 
of  the  deciduous  upper  central  incisors,  with  the  space  between 
the  lateral  incisors  being  occupied  by  only  one  peg-shaped  tooth. 
The  absence  of  teeth  from  the  arch,  (abnormalities  of  number) 
should  be  diagnosed  invariably  with  the  aid  of  carefully  secured 
radiograms.  Unquestionably,  many  cases  of  absence  of  teeth,  as 
reported  in  the  past,  have  been  cases  of  nqneruption  or  incarcer- 
ation of  fully  calcified  teeth  which  had  remained  within  the  sub- 
stance of  the  jaws;  in  some  cases  this  incarceration  did  not  cause 


Pig. 

cuspid. 


Noneruption     of     permanent  Fi 

cuspi< 


!3.      Noneruption     of     permanent 


any  apparent  discomfort  to  the  patient,  while  in  others  it  pro- 
duced reflex  manifestations  of  varying  degrees  of  intensity.  The 
third  molar  is  often  missing  which  is  due  almosl  invariably  to 
its  noneruption,  and  not  to  failure  either  of  calcification  of  the 
tooth  follicle,  or  to  the  evolution  of  the  tooth  germ. 

The  series  of  cases  of  noneruption  of  the  third  molar  which 
here  follow  belong  to  a  class  in  which  the  presence  of  abnormal 
degrees  of  irritation  in  the  jaws  brought  about  severe  nervous 
manifestations,  reflex  in  character.  The  conditions  encountered 
in  these  cases  indirectly  undermined  the  individual's  health, 
for  the  reason  that  continued  pain  acts  as  a  powerful  source  of 
inhibition  from  those  nervous  stimuli  which  are  indispensable 
for  the  continuance  of  all  vital  functions.     Pain,  regardless  of 


ABNORMALITIES    IN    THE    NUMBER    OF    TEETH 


295 


its  source,  gives  rise  to  functional  disturbances  proportionate  to 
its  degree  of  severity.  Tain  must  be  combated  witnoul  delay 
because  of  its  injurious  effect  upon  the  nervous  function.    So  well 


Fig. -224.' • 


Fig.  225. 


did  Soullier,  that  scholarly  therapeutist  of  Lyons,  appreciate  the 
significance  of  disturbed  functional  activity  caused  by  continued 
degrees  of  pain,  that  he  referred  to  this  symptom  as  being  to  the 
nervous  system  what  hemorrhage  is  to  the  vascular. 


2% 


DENTAL    PATHOLOGY 


Case  Histories 

A   young   woman,   twenty   years   of   age,   had   been    suffering   intense   pain 
for  a  period  of  several  months.     She  had  sustained  a  loss  in  weight  of  six- 


Fig!  226. 


Fig.  227. 

teen  pounds  in  six  weeks.  This  case  (Fig.  224)  showed  impaction  of  the 
upper  and  lower  third  molars.  Their  removal  was  followed  by  severe  post- 
operative pain,  but  three  weeks  afterward  she  had  regained  her  usual  nor- 
mal good  health. 


ABNORMALITIES    I N    THE    NUMBER    OF    TEETH 


297 


A  man  about  thirty-five  years  old  gave  a  history  of  tic  douloureux  of  fif- 
teen years'  standing.  The  x-ray  showed  an  impacted  lower  third  molar  on 
the  right  side,  which  was  removed,     [mprovemenl   followed. 

A  woman  gave  a  history  of  intense  pain  in  the  right  ear  of  ten  weeks' 
standing.  The  specialist  to  whom  she  was  referred  treated  her  for  otitis 
media.  As  a  measure  of  last  resort,  and  in  order  to  relieve  the  intensity  of 
her  suffering,  a  puncture  of  the  drum  was  made,  but  without  bringing  about 
the  much  sought-for  relief.  The  removal  of  an  impacted  right  third  molar 
(Fig.  225)  brought  about  complete  cessation  of  all  symptoms  in  one  week's 
time. 

A  girl,  aged  seventeen  years,  with  painful  reflexes  in  the  ear.  had  an  un- 
erupted  third  molar  removed  Fig.  226),  resulting  in  a  cure  within  six 
weeks  '  time. 

A  young  girl  complained  of  intense  pain   in  the  eyes  and  in   the  ear,  and 


Fig.  228. 


a  negative  history  of  painful  symptoms  in  the  teeth.  She  also  exhibited 
intense  mental  and  hysterical  symptoms.  The  pain  had  been  going  on  for 
a  period  of  three  years.  The  radiogram  showed  impacted  upper  and  lower  third 
molars  on  both  sides.  These  teeth  were  extracted,  and  while  there  were 
marked  postoperative  disturbances,  eventually  she  regained  her  normal  health. 

A  girl,  aged  nineteen  years,  with  painful  reflexes  localized  in  the  ear,  had 
the  upper  and  lower  impacted  third  molars  extracted,  and  recovery  soon  fol- 
lowed. 

Fig.  227  shows  the  mouth  radiogram  of  a  girl,  aged  seventeen,  giving  a 
history  of  severe  facial  pain.  The  second  bicuspid  and  second  molar  had 
failed  to  erupt  up  to  the  age  of  seventeen,  but  eventually  came  through  of  their 
own  accord. 


298  DENTAL   PATHOLOGY 

A  woman,  aged  forty-five  years,  gave  a  history  of  recurrent  dull  pain 
on  the  right  side  of  the  face  in  the  upper  and  lower  teeth.  The  radiogram 
(Fig.  228)  shows  an  impacted  lower  third  molar,  which  was  extracted.  There 
followed  a  complete  disappearance  of  the  painful  manifestations.  As  a  side- 
light on  the  influence  of  pathologic  condition  of  the  teeth  as  regards  defec- 
tive phonation,  this  patient  exhibited  a  peculiar  symptom:  when  she  called 
for  advice  and  treatment  her  voice  was  of  a  deep,  sonorous,  husky  type.  With 
the  extraction  of  the  offending  tooth,  the  charm  of  the  feminine  voice  re- 
turned. 


CHAPTER  XVII 

HUTCHINSON'S  TEETH  AND  OTHER  SYPHILITIC 
STIGMATA1 

Etiology. — The  transmission  of  syphilis  to  the  child  in  utero  is 
responsible  for  the  production  of  characteristic  malformations  in 
the  permanent  incisors,  cuspids,  and  first  molars,  and  in  the  de- 
ciduous second  molars.  Cavallaro2  has  investigated  the  dental  de- 
fects in  children  with  congenital  syphilis,  and  his  masterly  work 
offers  a  basis  for  accurate  deductions.  He  has  collected  a  large 
number  of  cases  bearing  on  the  question,  and  comes  to  the  con- 
clusion that  unquestionably  congenital  syphilis  produces  charac- 
teristic malformations  in  the  teeth. 

The  tooth  described  by  Jonathan  Hutchinson  when  considered 
alone,  can  not  be  pathognomonic  of  inherited  syphilis ;  but  when 
present  in  conjunction  with  other  dental  abnormalities,  and  with 
ocular  and  auricular  disturbances,  it  is  practically  without  ques- 
tion that  the  subject  so  affected  is  a  heredosyphilitic. 

The  deformities  of  the  teeth  to  which  Hutchinson  called  at- 
tention are  the  semilunar  defects  in  the  incisal  region  of  the 
upper  central  incisor.  The  tooth  is  narrower  at  the  incisal  edge 
than  at  the  neck,  is  a  smaller  organ  than  the  normal  tooth,  and 
is  accompanied  by  hypoplasia  of  the  cusps  of  the  first  molar.  It  is 
sometimes  found  in  the  upper  laterals,  the  lower  incisors,  and  ex- 
ceptionally in  the  cuspids  (Fig.  229).  The  tooth  is  not  always 
notched  incisally  upon  eruption,  but  acquires  that  characteristic 
after  it  undergoes  abrasion  consequent  upon  mastication.  The 
deformity  is  due  to  imperfect  calcification  of  the  incisal  end  of 
the  middle  lobe  of  the  incisor,  the  structure  occupying  the  site 
of  the  future  notch  being  delicate  and  imperfect  and  readily 
disappears  when  the  tooth  is  subjected  to  attrition  (Fig.  230). 
The    typical    so-called   Hutchinson's    tooth    is    not,    as    a    rule, 


'We  are  indebted  to  the  writings  of  Joseph  Cavallaro  in  the  Dental  Cosmos,  vols.  1 
and  li,   for  the   basic   facts   in   the  preparation   of   this   chapter. 

^Cavallaro,  Toseph :  Syphilis  in  Relation  to  Dentition,  Dental  Cosmos,  1908,  Nos.  11 
and  12;     and  1909,  Nos.   1  and  2. 

299 


800 


DENTAL   PATHOLOGY 


Fig.    229. — Hutchinson's    teeth.      Sulciform    erosions    of   incisors.      Diastema.      (Cavallaro.) 


Fig.  230. — Hutchinson  teeth.     Cuspal  erosions   of  canines  and   molars.     (Cavallaro.) 


HUTCHINSON  S    TEETH    AM)    SYPHILITIC    STIGMATA 


.301 


observable  after  the  thirtieth  year,3  since  the  mesial  and  distal 
lobes  undergo  abrasion,  and  the  incisal  edge  becomes  very  nearly 
straight,   although    a   semilunar  marking   may    persisl    above   the 


Fig.  231. — Hutchinson's  teeth.  Cuspal  atrophy  of  canines  and  first  molars.  Sulciform 
erosions  of  lower  incisors.  Vertical  grooves.  Diastema.  Cup-shaped  erosions  of  the 
persistent    lower   left   deciduous    molar.       (Cavallam.  > 


Fig.   232. — Multiple  sulciform  erosions,  general,  and   involving  the  bicuspids.      (Cavallaro.) 


Fig.    233. — Lingual    aspects   of   preceding    illustrations.      Hutchinson's    teeth.       (Cavallaro.) 


3Cavallaro,   Joseph:      L,oc.    cit. 


302 


DENTAL   PATHOLOGY 


abraded  incisal  edge.  It  usually  affects  both  central  incisors,  one 
central  alone  rarely  being  affected.  Fournier,  cited  by  Cavallaro, 
has  reported  a  case  of  congenital  syphilis  in  which  the  cutting  edges 
of  the  upper  central  incisors,  the  lower  central  incisors,  and  one 
cuspid  had  "well-marked  crescentic  notches."  The  Hutchinson 
sign  refers  particularly  to  the  semilunar  or  crescentic  notch  on 
the  incisal  edge  in  the  upper  or  lower,  or  both,  central  and  lateral 
incisors  and  cuspids. 

The  dental  apparatus  may  be  affected  in  many  other  ways  as 


Fig.   234. — Hutchinson    teeth.      Honeycomb   erosions.      (Cavallaro.  ) 

the  result  of  nutritional  disturbances  induced  by  the  presence 
or  introduction  of  the  syphilitic  virus  into  the  child  (Figs.  231 
to  236).  To  this  source,  among  many  others,  but  not  exclusively, 
may  be  traced  the  tardy  decalcification  of  the  deciduous  teeth, 
and  the  correspondingly  late  eruption  of  their  permanent  suc- 
cessors; the  absence  of  certain  teeth,  such  as  the  upper  lateral 
incisors,  or  the  lower  bicuspids;  the  development  of  a  tooth  in  an 
abnormal  location,  i.e.,  under  the  tongue,  in  the  maxillary  sinus, 


in  Trill. \ son  s  ti;i:th  and  syphilitic  stigmata 


303 


in  the  hard  palate,  vomer,  nasal  fossae,  sphenoid,  inferior  orbital 
margin,  stomach,  ovaries,  and  in  dermoid  cysts;  supernumerary 
teeth;  underdevelopment  of  the  jaws;  and  V-shaped  palate,  cleft 
palate,  and  harelip.4 

Cavallaro  considers  that  the  Hutchinson's  semilunar  notching, 
particularly  of  the  incisors,  is  "pathognomonic  of  hereditary 
syphilis  in  at  least  50  per  cent  of  cases,"  and  as  his  opinion  is 


Fig.    235. — Hutchinson    teeth.      Microdontism.     (Cavallaro.) 


Fig.    236. — Complete   congenital   absence   of  teeth   in   the    upper   arch.    (Cavallaro.) 

sustained  by  Fournier,  whose  experience  as  a  syphilographer  is 
far-reaching,  statements  to  the  contrary  by  observers  of  only 
limited  experience  should  carry  very  little  weight.  Cavallaro 's 
conclusions  here  follow  :5 

"1.  In  heredosyphilitics  the  following  various  dental  stigmata 
are  found :  erosions  of  the  crown,  cuspal  erosion,  and  Hutchin- 
son's teeth;  white  sulci;  white  marks;  delay  of  development  and 


4Loc.  cit. 

5Cavallaro,  Joseph:     Syphilis  in  Relation  to  Dentition,  Dental  Cosmos,  February,   1909. 


304  DENTAL   PATHOLOGY 

eruption;  dental  infantilism;  microdontism ;  amorphism;  per- 
sistence of  the  deciduous  teeth;  anomalies  of  structure,  shape, 
number,  direction,  arrangement  and  color ;  vulnerability  of  the 
dental  system;  ectopia  (malpositions'),  total  or  partial  absence 
of  teeth,  wearing  away,  premature  caries,  premature  loss  of  teeth, 
spaces  between  teeth  (diastema),  and  the  following  maxillary 
stigmata :  malocclusion,  defective  articulation  of  the  dental 
arches,  prognathism,  ogival  palate  and  cleft  palate. 

"2.  The  dental  stigmata  are  the  most  frequent  characteristic, 
being  persistent  and  indelible  among  the  stigmata  of  hereditary 
syphilis. 

"3.  The  erosions  are  systematic;  they  occupy  the  same  level  on 
homologous  teeth,  and  a  different  one  on  teeth  of  a  different 
order  (showing  their  relative  periods  of  calcification).  Besides, 
they  have  a  marked  predilection  for  some  teeth  (Hutchinson's 
erosion  in  the  upper  centrals,  horizontal  grooves  in  the  lower  in- 
cisors, and  cuspal  atrophy  in  the  canines  and  first  molars). 

"4.  The  dental  stigmata  do  not  belong  exclusively  to  the  sec- 
ond, but  are  also  frequently  found  in  the  first  dentition.  Some 
cases  of  dental  stigmata  in  the  third  generation  have  been  re- 
corded. 

"5.  The  cup-shaped,  or  honeycomb,  erosion  on  the  deciduous 
molars,  especially  on  the  second,  is  very  frequent. 

"6.  The  dental  alterations  as  found  in  idiots,  backward  chil- 
dren, etc.,  represent  a  type  quite  different  from  those  found  in 
hereditary  syphilitic  subjects.  Hutchinson's  teeth,  the  systemic, 
lesions,  the  horizontal  grooves,  dental  infantilism,  and  the  cup- 
shaped  erosion  in  the  deciduous  molars,  are  peculiar  to  hereditary 
syphilitic  subjects,  while  in  idiots  the  vertical  grooves  are  noted. 

"7.  The  dental  stigmata  are  rarely  found  alone  (we  have  ob- 
served only  three  out  of  fifty-six  eases) ;  they  are  generally  as- 
sociated with  other  stigmata  of  the  head  or  with  other  general 
concomitant  stigmata. 

"8.  A  relationship  between  the  factors  of  Hutchinson's  triad 
(a  syndrome  of  congenital  syphilis — Hutchinson  teeth,  otitis 
media,  and  diffuse  interstitial  keratitis),  especially  between  the 
dental  and  the  ocular  lesions,  is  very  frequently  found. 

''In  fifty-six  cases  of  dental  lesions  ocular  lesions  were  found 
thirty-five  times,  and  auricular  lesions  twelve  times. 


Hutchinson's  teeth  and  syphilitic  stigmata  305 

"9.  The  anatomic  and  pathologic  examination  of  the  dental 
follicles  of  syphilitic  teeth  furnishes  us  with  the  following  char- 
acteristic symptoms:  constrictions,  which  clinically  eorrespond 
to  the  euspal  atrophies;  alterations  of  the  enamel  and  dentin,  in- 
terprismatic  spaces,  interglobular  spaces,  rounded  islands,  granu- 
lations due  to  an  inhibitory  disturbance  which  acted  upon  the 
tissues  during  the  period  of  development. 

"10.  In  the  dental  follicles  of  macerated  and  doubtless  syphi- 
litic fetuses  the  following  alterations  have  been  found:  Endo- 
vasculitis.  perivasculitis,  hemorrhage  and  parvicellular  infiltra- 
tion. 

"11.  Tin'  Spirochete  pallida  is  abundantly  found  in  the  dental 
follicle  near  the  so-called  dentinal  cap.  in  proximity  to  the  ves- 
sels, and  in  their  Avails. 

"12.  The  dental  stigmata  depend  upon  a  general  morbid 
cause,  which  manifests  its  inhibitory  action  during  the  period  of 
development  of  the  tooth,  i.e.,  the  second  half  of  intrauterine  life 
and  the  first  months  of  extrauterine  life.  Such  a  morbid  general 
cause  can  be  only  syphilis. 

"13.  The  presence  of  vascular  alterations  and  of  the  Spirocheta 
pallida  in  the  dental  tissues  leads  us  to  believe  that  the  dental 
stigmata  are  of  syphilitic  nature  and  not  of  indirect  syphilitic 
origin  only. 

"14.  The  dental  stigmata  are  of  great  importance  for  the  diag- 
nosis of  hereditary  syphilis,  indicating  the  disease  even  before 
the  appearance  of  other  stigmata. 

"Hutchinson's  teeth,  the  euspal  atrophy  of  the  first  perma- 
nent molar,  the  multiple  systemic  lesions  of  the  second  dentition, 
the  multiple  and  systemic  lesions  of  the  first  dentition,  especially 
the  cup-shaped  erosions  of  the  molars,  are  pathognomonic  of 
hereditary  syphilis.  In  twenty-three  out  of  fifty-six  cases  Hutch- 
inson's teeth  have  been  found. 

"15.  The  maxillary  alterations,  although  frequently  found  in 
hereditary  syphilitic  subjects,  do  not  possess  an  absolute  diag- 
nostic value. 

"16.  The  specific  treatment  is  always  to  be  suggested  in  hered- 
itary syphilitic  children  with  dental  stigmata,  even  if  these 
stigmata  are  found  alone  and  unassoeiated  with  other  syphilitic 
or  dystrophic  stigmata. 


CHAPTER  XYIII 

DENTAL  CARIES 

Historical  Data 

The  destruction  of  the  hard  tissues  of  the  tooth,  commonly 
called  caries,  or  decay,  has  been  the  subject  of  considerable  specu- 
lation as  to  its  etiology  and  pathology  in  ancient,  as  well  as  com- 
paratively modern  times.  Scores  of  theories  are  on  record  in  the 
literature  of  the  subject,  some  writers  having  adhered  to  as  many 
as  two  or  three  of  them,  all  to  be  discarded  upon  the  publication  by 
W.  D.  Miller  of  his  epoch-making  writings  on  the  production  of 
caries  in  vitro.  The  Egyptian  skulls  of  the  period  around  450  b. 
c.  show  no  evidence  of  any  systematized  attempt  having  been  made 
in  those  prehistoric  times  at  filling  cavities  of  decay,  although 
a  few  skulls  have  been  unearthed  with  gold  incrustations  in  the 
occlusal  surfaces,  leading  to  the  supposition  that  some  of  the  an- 
cient Egyptians  had  some  inkling  as  to  the  need  of  repairing  by 
artificial  means  the  destruction  wrought  by  caries.  By  inference 
it  may  be  concluded  that  not  even  the  earliest  of  races  were  free 
from  the  ravages  of  dental  decay.  Hippocrates,  a  Greek  physician, 
who  lived  some  five  centuries  before  Christ,  thought  that  caries 
was  a  manifestation  of  "stagnation  of  depraved  juices."  This 
theory,  or  a  modification  of  it,  persisted  for  centuries,  even  up  to 
the  end  of  the  eighteenth  century.  A  certain  phlegm  under  the 
roots  of  teeth  was  considered  by  him  as  the  cause  of  caries.  But 
particularly  interesting  is  his  statement  that  food  debris  is  a 
cause  of  caries  which  attacks  the  weakest  and  less  adherent  teeth. 
As  late  as  the  latter  part  of  the  eighteenth  century  this  theory  was 
exploited  by  Bourdet  (1757),  by  Benj.  Bell  (1787),  and  Serre 
(1788). 1 

Cornelius  Celsus,  the  Roman  physician,  born  some  twenty-five 
years  before  the  Christian  era,  was  aware  of  the  existence  of  a 
malady  which  caused  the  formation  of  cavities  in  the  teeth. 


1Miller,    W.    D.:      Microorganisms    of    the    Human    Mouth,    S.    S.    White    Dental    Mfg. 
Co.,  Philadelphia. 

306 


DENTAL    CAK 1 1  B  307 

Scribonius  Largus,  a  contemporary  of  Emperor  Claudius,2  in 
tlic  middle  of  the  firsl  century  was  the  author  of  a  conception  of 
caries  which  persisted  for  centuries:  It  was  to  worms  which  grew 
in  the  teeth  and  gnawed  away  their  substance  that  the  cause  of  the 
disease  was  attributed.  The  worm  theory  of  caries  was  accepted 
and  promulgated  by  Musitanus  of  Naples  (1635-1711),  Krauter- 
mann  (1766-1854),  and  Ringelmann  (1821). 3  In  this  connection 
Scribonius  admonished  that  "there  are  those  who  pretend  that 
the  forceps  is  the  only  remedy  for  odontalgia.  Nevertheless,  be- 
t'.>re  resorting  to  this  extreme  measure,  other  means  can  be  uti- 
lized. When  a  portion  of  the  tooth  is  decayed,  I  advise  that  it  be 
scratched  with  the  excavator  (scalprum  medicinale).  The  opera- 
tion is  not  painful  and  the  remainder  of  the  tooth  will  render  the 
same  service  as  the  whole  tooth.  If  the  pain  persists,  one  should 
have  recourse  to  collutories,  to  substances  to  be  chewed,  to  fumiga- 
tions, to  dentifrices." 

The  art  of  filling  teeth  with  metallic  substances  was  unknown  to 
the  Romans;  but.  on  the  other  hand,  they  advised  filling  the 
cavities  with  a  powder  made  of  the  excrements  of  mice  or  the 
livers  of  lizards  and  covering  the  filling  with  wax. 

Archigenes,  toward  the  end  of  the  first  century,  was  particularly 
concerned  in  devising  remedies  against  odontalgia,  and  combina- 
tions to  be  introduced  into  carious  teeth,  doubtless  to  control  the 
pain  associated  with  pulpitis. 

Galen,  a  physician  who  lived  in  the  year  131  a.d.,  and  later  on 
Acetious  of  Amida.  in  550  a.d.,  believed  that  caries  was  caused  by 
disturbances  of  nutrition  which  produced  vicious  humors  which 
should  be  allowed  to  desiccate.  Again,  that  caries  was  the  result 
of  an  inflammation  of  the  dentin  was  advanced  by  Galen,  Eus- 
tachius  (1571),  John  Hunter  (1788),  Joseph  Fox  (1806),  and 
Thos.  Bell  (1831.) 4  The  inflammation  theory  of  caries  was  revived 
in  1889  by  Heitzman,  Bodecker.  and  Frank  Abbott  of  New  York. 

In  the  Middle  Ages.  Rhazes,  born  in  Persia  in  850  a.d.,  thought  of 
caries  as  a  process  similar  to  the  understanding  which  they  had  at 
that  time  of  the  gradual  destruction  of  bone  (caries  of  bone). 
Rhazes  knew  that  acids  had  a  destructive  action  upon  the  teeth. 


2Lemerle,  L  :      Xotice  sur  L'Histore  de  1'  Art   Dentaire. 
3Miller:     Loc.   cit. 
4Miller:      Loc.   cit. 


308  DENTAL    PATHOLOGY 

Ali  Abbas5  aboul  the  year  L094,  a.d.,  in  a  voluminous  treatise  of 
medicine,  mentions  a  number  of  diseases  of  the  teeth,  with  cor- 
rosion, or  caries,  among  them. 

Avicenna  980-1037),  a  Persian  physician,  the  author  of  the 
Canon,  and  recognized  by  his  contemporaries  as  the  "prince"  of 
physicians,  attributed  destructive  action  to  the  dentifrices  of  thai 
time,  claiming  that  their  eausticity  injured  the  substance  of  the 
teeth.  He  also  admonished  his  readers  thai  the  narcotics  used 
for  toothache  injured  the  teeth.  Avicenna  formulated  certain 
rules  for  the  prevention  of  dental  disease.  [fe  recommended  that 
certain  articles  of  food  which  he  conceived  as  being  capable  of 
undergoing  putrefaction  be  eliminated  from  the  diet,  viz..  fish 
and  milk:  avoidance  of  too  hot  or  too  cold  beverages,  particu- 
larly one  after  the  other;  avoidance  of  chewing  hard  substances, 
such  as  hour  or  sticky  foods,  viz..  figs  and  sweets;  avoidance  of 
meats  which  injure  the  teeth;  avoidance  of  contrivances  for  pick- 
ing the  teeth:  and  as  a  remedy  againsl  dental  ills,  rubbing  them 
with  honey  and  burnt  salt. 

Abulcasis,  the  author  of  the  Altasrif,  a  treatise  on  surgery 
which  appeared  at  the  beginning  of  the  tAvelfth  century,  devotes 
several  sections  of  the  book  to  dental  disease. 

Giovanni  d'  Arcoli  (John  Arculannus),  professor  at  Bologna. 
studied  the  means  of  arresting  the  ravages  of  caries.  He  recom- 
mended cleaning  the  cavity  with  acids  and  filling  it  with  sheets 
of  gold.  Arculannus  was  apparently  the  first  to  suggest  the  fill- 
ing of  teeth  with  gold  foil  in  the  year  1450.  In  1470  John  Pla- 
tearius,  professor  at  Pisa,  revived  the  worm  theory  of  caries. 
This  was  the  theory  accepted  by  Tlyff.  who  lived  in  the  latter  part 
uf  the  fifteenth  century  and  died  about  1571.  Lazare  Riviere5  of 
Montpellier,  professor  of  chemistry,  also  appears  to  have  ad- 
hered to  the  worm  theory  of  caries  and  recommended  certain 
substances  to  destroy  them.  Ambroise  Pare,  a  famous  French 
physician  and  surgeon  of  the  sixteenth  century,  discusses  cer- 
tain diseases  of  the  teeth  in  a  book  published  in  1560;  but  his 
theories  of  caries  are  just  as  impossible  as  those  of  his  prede- 
cessors, whose  views  we  have  already  recorded.  lie  leans  to- 
ward  the   theory   of   vicious   humors   as   expounded   by   Hippoc- 


5Lemcrlc,  L. :     Notice  sur  1'  Ilistoire  de  1'  Art  Dentaire. 


DENTAL   CARIES  300 

rates   and    Galen    twenty   and    fourteen    centuries,   respectively, 

previously. 

Pierre  Fauchard,  a  French  dentist  and  writer  who  lived  in  the 
latter  pari  of  the  seventeenth  and  the  first  part  of  the  eighteenth 
century  (1728),  made  efforts  to  find  the  worms  that  had  been 
considered  by  his  predecessors  as  the  cause  of  decay,  hut  he,  as 
well  as  Pfaff,  a  German  dentist  (1756),  failed  to  locate  these 
animalcules,  and  abandoned  the  worm  theory.  Thereafter,  to 
Fauchard,  "caries  was  produced  by  a  humor  which  finds  its  way 
into  the  osseous  fibers  of  the  tooth,  or  by  a  depraved  saliva,  or  by 
rough  foods,  or  by  certain  eroding  substances  placed  upon  the 
teeth  to  cure  or  bleach  them.  The  internal  causes  are  contained 
in  the  blood  by  making-  it  less  fluid  and  causing  it  to  form  ob- 
structions in  the  vessels  of  small  diameter.  The  teeth  are  more 
subject  to  caries  than  the  other  bones  of  the  body  because  their 
tissues  are  closer  together,  which  explains  their  obstruction  and 
strangulation." 

The  putrefaction  theory  of  decay  was  described  by  Pfaff,  but, 
of  course,  we  know  now  that  a  tooth  may  remain  for  any  length 
of  time  in  a  putrefying  mass  without  the  enamel  being  thereby 
affected.  The  electrical  theory  of  decay  was  also  in  vogue  for 
some  time,  and  was  championed  by  Bridgeman  before  the  Odon- 
tological  Society  of  Great  Britain  in  1861.  John  Hunter  (1728- 
1793),  in  his  famous  book  published  in  1771,  in  which  he  dis- 
cusses the  anatomy  and  diseases  of  the  teeth,  admits  that  caries 
is  a  disease  of  obscure  origin  and  not  caused  by  external  irrita- 
tion or  chemical  processes. 

Neither  Jourdain  (1734-1816),  writer  and  dentist,  nor  Bourdet 
(1757),  writer  and  dentist,  added  anything  to  the  notions  in 
vogue  in  those  times  concerning  caries.  Berdmore,  in  1771,  was 
the  first  to  investigate  the  action  of  nitric  and  sulphuric  acids 
upon  the  teeth ;  to  sour  food  and  to  acids  an  injurious  action  had 
been  attributed  back  in  1677  by  Paseh.  One  of  the  most  pro- 
lific writers  upon  the  subject  of  the  chemical  cause  of  caries  was 
Magitot.  Tomes,  in  1873,  reached  the  noteworthy  conclusion 
that  caries  is  the  effect  of  external  causes  in  which  so-called  vital 
forces  play  no  part ;  and  that  caries  is  due  to  the  action  of  acids 
that  have  been  generated  by  fermentation  in  the  mouth;  but  at 
that  time  Tomes  attributed  no  importance  to  the  agencies  through 


310  DENTAL   PATHOLOGY 

which  this  acid  was  generated  in  the  mouth.  In  more  recent  times 
Jonathan  Taft  was  a  strong  advocate  of  the  chemical  theory. 
Magitot  was  able  to  produce  artificial  cavities  in  extracted  teeth 
by  the  action  of  the  products  of  the  fermentation  of  sugar,  as 
well  as  with  several  acids.  The  chemical  theory  alone,  however, 
does  not  explain  all  the  phenomena  concerned  in  dental  caries. 
The  chemicoparasitic  theory,  the  one  to  which  we  adhere  today, 
was  brought  out  to  some  extent  by  Leber  and  Rottenstein  in  1867. 
W.  J.  Milles  and  A.  S.  Underwood,  in  1881,  before  the  Dental 
Section  of  the  International  Medical  Congress  of  London,  reported 
in  a  paper  on  the  "Nature  of  Dental  Caries"  the  constant  pres- 
ence of  microorganism  in  tooth  decay,  and  the  widening  of  the 
tubules  produced  by  microorganisms.  Milles  and  Underwood 
should  be  credited  with  the  first  microscopic  demonstration  of  the 
bacterial  causation  of  dental  caries.  Their  opinion  was  to  the 
effect  that  the  acid  that  dissolved  the  enamel  was  secreted  by  the 
bacteria.  It  remained  for  Miller  to  clarify  the  situation,  which  he 
did  following  a  series  of  painstaking  investigations  resulting  in 
the  production  of  artificial  caries  in  the  laboratory  identical  in 
etiology  and  pathologic  lesion  with  caries  as  it  develops  in  the 
teeth  of  man. 

Miller's  theory,  as  accepted  today,  is  to  the  effect  that  caries  of 
the  enamel  consists  in  its  entirety  of  the  dissolution  of  the  enamel 
by  lactic  acid  formed  in  situ  by  th(  fermentation  of  carbohydrates 
which  adhere  to  the  surface  of  the  enamel;  and  that  caries  of  den- 
tin and  cementum  consists  of  two  distinct  steps:  (1)  the  dissolu- 
tion of  the  inorganic  salts  from  these  tissues,  and,  (2)  a  subsequent 
action  by  proteolytic  bacterial  enzymes  upon  the  organic  constit- 
uent of  the  dentin  and  cementum  of  the  tooth. 


CHAPTEE  XIX 
DENTAL  CARIES  (Cont'd) 

General  Considerations 

Dental  caries  is  the  most  widely  distributed  disease  of  mankind. 
Peoples  of  all  countries  and  races  are  subject  to  its  ravages, -and 
have  been  for  all  time,  since  caries  lesions  have  been  discovered  in 
exhumed  skulls  of  all  ages.  In  some  localities  and  among  certain 
peoples  it  occurs  with  greater  frequency  and  intensity  than  in 
others,  but  everywhere  it  is  to  be  found.  It  has  been  estimated  that 
from  85  to  95  per  cent  of  the  people  of  the  civilized  races  suffer 
from  caries. 

There  seems  to  exist  a  direct  relation  between  the  progress  of 
civilization  and  the  increase  in  the  prevalence  of  dental  caries.  In 
the  less  civilized  and  barbaric  tribes  the  prevalence  of  caries  is 
small;  in  the  highly  civilized  peoples  the  percentage  rises  tremen- 
dously. In  prehistoric  times  the  percentage  of  carious  teeth  varied 
from  as  low  as  2  per  cent,  or  less,  to  about  7  per  cent ;  in  contem- 
poraneous times,  and  among  the  most  highly  civilized  people,  par- 
ticularly, the  percentage  rises  to  95  per  cent  and  even  higher.  "With 
the  advance  in  civilization  there  has  occurred  a  gradual,  though 
radical  change  in  the  dietaries  of  men,  and  whereas,  in  prehistoric 
and  ancient  times  the  character  of  the  food  was  such  as  to  act  as 
a  cleanser  or  detergent  of  tooth  surfaces,  and  as  a  stimulus  to  the 
growth  of  the  jaws  leading  to  regularity  of  position  of  the  teeth  in 
the  arch,  in  modern  times  the  food,  being  of  the  soft  and  mushy 
variety,  has  a  tendency  to  become  lodged  upon  the  surface  of  the 
enamel,  and  affords  little  stimulation  to  the  development  of  the 
jaws.  The  consequence  is  that  the  teeth  are  malposed  in  the  arch 
and  strongly  predisposed  to  dental  caries.  Pickerill  attributes  the 
immunity  to  caries  among  the  uncivilized  tribes  of  the  world  not 
to  an  excessive  protein  diet  and  a  small  carbohydrate  intake — for  he 
tells  us  that  the  dietaries  of  the  uncivilized  tribes  do  not  necessarily 
consist  of  protein  substances  only,  but  that  they  are  decidedly  of  a 
mixed  character.     He  attributes  the  immunity  from  caries  to  the 

311 


312  DENTAL   PATHOLOGY 

use  of  salivary  stimulants — fruits  with  their  fruit  acids,  acid  or 
pungent  plants,  sour  foods,  etc. — and  masticatories,  viz.,  gums  of 
different  trees  which,  when  chewed,  stimulate  the  flow  of  saliva  and 
therefore  increase  diastatic  action.  No  importance  is  attributed 
hy  Pickerill  to  the  use  of  coarse  fibrous  foods  as  detergents  in  the 
case  of  the  immune  races,  for  again  he  assures  us  that  in  the  case 
of  the  Maori,  and  other  similar  races,  nearly  all  food  is  steamed, 
thus  considerably  reducing  its  toughness.  Be  that  as  it  may,  wo. 
are,  however,  satisfied  that  the  character  of  the  food  per  se  is  of 
paramount  importance  in  maintaining  the  surface  of  the  enamel 
free  from  the  sticky  coatings  so  evident  in  mouths  of  the  caries  sus- 
ceptibles.  The  views  of  Bunting6  are  here  quoted  in  corroboration 
of  the  belief  that  the  nature  of  the  foods  ingested  has  a  bearing 
upon  the  production  of  dental  caries.  He  says,  "It  is  very  evident 
that  certain  forms  of  carbohydrates  have  a  greater  tendency  to 
stick  to  the  teeth  than  others.  The  soft  sticky  varieties  of  sugars 
and  cooked  starches,  which  are  slowly  soluble,  are  especially  liable 
to  retention,  and  form  favorable  pabulum  for  acid  fermentation. 
That  the  continued  and  copious  diet  of  such  substances  is  favor- 
able to  caries  can  not  be  doubted.  The  mouths  of  candy-makers, 
millers,  and  children  who  eat  largely  of  sweets,  are  strong  in  the 
corroboration  of  this  view.  And  conversely,  we  know  that  the 
Eskimo  and  the  meat-eating  tribes  of  South  America,  who  have 
little  or  no  carbohydrate  in  their  diet  are,  as  a  race,  remarkably 
free  from  caries." 

The  presence  of  salivary  stimulants  in  the  diet  of  the  immune 
races,  and  their  absence  from  the  diet  of  the  civilized  races,  un- 
doubtedly plays  an  important,  but  not  exclusive,  role  in  the  deter- 
mination of  susceptibility  and  immunity.  Pickerill,  whose  investi- 
gations on  the  dietaries  of  the  immune  and  susceptible  races  in  their 
relation  to  dental  caries  constitute  a  most  complete  and  depend- 
able study  on  the  subject,  traces  the  lack  of  immunity — the  high 
susceptibility  to  dental  caries — to  dietaries  which  contain  an 
abundance  of  food  articles  which  act  as  salivary  depressants  and 
which  are  of  Ititjh  potential  acidity.  Some  of  his  conclusions  con- 
cerning the  prevalence  of  caries  among  the  civilized  and  uncivi- 
lized races  are  quoted  here  in  further  elucidation  of  the  subject: 

1.  That  the  number  of  persons  affected  with  dental  caries  who 


eBunting:      Journal    of   the    National    Dental   Association. 


DENTAL    CARIES  313 

live  under  uncivilized  or  "natural"  conditions  is  comparatively 
small  varying  from  1  to  20. S  per  cent,  while  in  civilized  modern 
races  the  percentage  is  as  high  as  98  per  cent,  the  increase  being 
at  Least  77.4  per  cent. 

2.  That  the  number  of  teeth  affected  with  caries  in  each  individ- 
ual is  far  less  in  those  leading  natural  lives  than  in  those  leading 
artificial  or  highly  civilized  lives,  in  the  former  varying  from  2  to 
7  per  cent,  while  in  the  latter  it  has  become  as  high  as  from  15 
to  52  per  cent,  showing  a  maximum  increase  of  45  per  cent. 

3.  That  in  the  British  races,  which  have  been  subject  to  the  in- 
fluence of  civilization  for  nearly  2,000  years,  the  increase  in  the 
percentage  of  caries  is  about  79  per  cent.  This  corresponds 
closely  to  the  difference  in  percentage  given  above  in  1. 

4.  That  in  the  Maori  race,  which  has  been  subject  to  the  in- 
fluences of  civilization  for  only  seventy  or  eighty  years  at  the 
very  most,  but  has  only  become  "civilized"  in  habits  quite  re- 
cently, the  increase  is  93  per  cent.  (But  against  this  apparently 
high  figure  has  to  be  set  the  fact  that  the  incidence  of  caries  in 
each  mouth  is  comparatively  low.) 

Caries  is  a  disease  which  has  kept  up  its  ratio  of  increase  with 
advancing  civilization.  J.  R.  Mummery,7  for  instance,  tells  us 
that  in  the  series  of  skulls  of  the  primitive  races  examined 
by  him  the  percentage  which  showed  carious  teeth  varied  from 
1.4  in  the  Eskimo  to  20.8  in  the  negro  (slaves)  ;  in  the  civilized 
races  this  ratio  has  increased  tremendously.  In  English  and 
Scotch  school  boys  and  girls,  in  a  series  of  10,500  individuals, 
the  presence  of  carious  teeth  was  found  in  86  per  cent  of  the 
cases;  in  the  children  of  Leith  the  percentage  was  98.60.  The 
percentage  among  American  school  children,  while  not  nearly  so 
large  as  among  European  school  children,  is  nevertheless  alarm- 
ingly high. 

In  a  series  of  cases  examined  by  Emerson,  out  of  1478  children 
from  one  to  fifteen  years  of  age,  81.2  per  cent  had  carious  teeth. 
In  this  percentage,  namely  1200  children,  5996  decayed  teeth 
were  found,  which  is  an  average  of  5.0  teeth  for  each  one  of  the 
1200  children,  or  4.7  teeth  for  each  one  of  the  1478  individuals 
examined.  These  children  were  not  suffering  from  any  acute 
disease,   although  their   general  health  was  failing   on   account 


transactions   of  the   Odontological    Society   of   Great   Britain. 


314  DENTAL   PATHOLOGY 

of  sickness  during  the  winter  previous  to  the  examination, 
and  also  on  account  of  various  forms  of  malnutrition,  anemia, 
and  general  debility,  all  doubtless  traceable  to  the  oral 
infection  present.  Of  634  cases  over  fifteen  years  of  age,  also 
in  indifferent  health,  probably  on  account  of  unhygienic  living, 
only  19,  or  3.0  per  cent,  had  no  defective  teeth;  this  leaves  615, 
or  97  per  cent,  in  whom  were  found  4022  decayed  teeth,  or  an 
average  of  6.5  teeth  for  each  of  the  634  children  examined.  In 
this  same  group  of  634  individuals,  1655  teeth  were  missing,  and 
in  addition  1444  artificial  teeth  were  present,  making  a  total  of 
3099  teeth  which  had  been  presumably  removed  for  advanced 
caries,  or  an  average  of  4.8  per  cent  for  each  one  of  the  634. 

There  are  so  many  factors  which  favor  the  development  and 
progress  of  caries  that  where  some  are  lacking,  others  are  pres- 
ent to  favor  its  progress.  From  the  time  a  tooth  makes  its  ap- 
pearance through  the  gum,  and  throughout  the  life  of  the  in- 
dividual, it  is  exposed  to  the  conditions  which  bring  about  caries, 
although,  of  course,  there  are  periods  when  the  teeth  are  more 
susceptible  to  caries  than  at  others,  as  well  as  periods  of  com- 
plete, or  almost  complete,  immunity.  The  amount  and  composi- 
tion of  the  saliva ;  the  position  of  the  teeth  in  the  arch  and  their 
relation  to  their  antagonists;  the  structural  peculiarities  of  the 
enamel  and  of  the  dentin;  the  character  of  the  diet;  the  general 
health  status;  and  the  degree  of  hygienic  care,  if  any — these 
alone  or  in  combinations,  are  at  the  bottom  of  the  caries  problem. 
There  was  a  time  when  it  was  assumed  that  cleanliness  of  the 
teeth  was  the  most  powerful  and  only  weapon  in  the  prevention 
of  caries;  but  today  we  must  conclude,  in  the  face  of  observations 
that  have  been  made  in  this  and  other  countries,  that  the  constitu- 
tional factor  can  not  be  altogether  eliminated  from  the  discussion 
of  the  subject  any  more  than  it  can  from  pyorrhea  alveola ris, 
or  from  diseases  of  the  eye,  throat,  nose,  skin,  etc.  These  ob- 
servations concerned  themselves  with  the  marked  tendency  to 
dental  caries  in  some  mouths  which  were  maintained  at  all  times 
in  a  state  of  scrupulous  cleanliness,  as  well  as  with  the  absence 
of  caries  in  certain  other  instances  of  badly  neglected  mouths. 

The  chemicobacterial  theory  of  Miller,  promulgated  by  him  in 
1882,  has  stood  the  test  of  scientific  inquiry  all  this  time ;  and  while 
it  explains  the   modus   operandi  of  dental   caries  with  scientific 


DENTAL    CARIES  315 

exactness,  still,  certain  important  phases  of  the  problem  of  dental 
caries  remain  as  yet  to  be  explored.  We  know  how  a  tooth  decays 
in  the  presence  of  carbohydrate  deposits  upon  its  surfaces,  with 
their  subsequent  fermentation,  with  lactic  acid  as  the  end-prod- 
uct; but  we  do  not  know  why  caries  is  rampant  in  some  mouths 
and  absent  in  others,  under  apparently  identical  conditions  of 
health,  diet,  climate,  living  quarters,  dental  hygiene,  etc.  Is  it 
the  composition  of  the  salivary  secretion?  The  evidences  ad- 
duced so  far  concerning  the  individual  constituents  of  the  saliva 
in  the  role  of  induction  or  prevention  of  caries,  does  not  clear 
the  question  to  any  great  extent.  The  sulphocyanate  content, 
for  instance,  bears  no  relation  to  the  subject,  as  shown  by  Gies, 
Howe,  Bunting,  and  others. 

Bearing  on  the  question  of  the  immunizing  properties  of  the 
saliva,  Miller's  studies  throw  considerable  light  on  certain  phases 
of  the  question,  although  with  negative  results.  Considering  a 
possible  similarity  between  the  hemolytic  power  of  the  blood 
serum  and  the  substances  which  are  introduced  into  the  body 
when  the  individual  is  immunized,  experiments  were  conducted  in 
order  to  ascertain  whether  the  saliva  has  any  hemolytic  action. 
These  experiments  show  that  fresh  saliva  brings  about  an  im- 
mediate total  solution  of  blood  cells,  but  that  this  action  is  not 
due  to  any  substance  contained  in  the  saliva,  but  to  its  water 
content,  as  proved  by  the  fact  that  0.75  per  cent  of  sodium 
chloride,  when  added  to  the  saliva  (i.e.,  an  isotonic  saliva  solu- 
tion), does  not  hemolyze  the  red  blood  cells  of  the  rabbit.  That 
the  saliva  has  practically  no  antiseptic  power  whatsoever,  has 
also  been  conclusively  shown,  inasmuch  as  microorganisms  re- 
tain their  virulence  in  the  presence  of  human  saliva.  Miller  also 
attacked  the  problem  of  caries  immunity  and  susceptibility  from 
the  standpoint  of  the  number  of  bacteria  in  the  mouth,  but  his 
experiments  show  that  the  saliva  of  those  immune  to  caries  con- 
tains almost  as  many  organisms  as  the  saliva  of  those  having 
moderate  caries,  or  even  those  who  are  highly  susceptible  to  the 
process.  He  says:  "The  saliva  of  immunes  develops,  in  the 
presence  of  carbohydrates  in  and  out  of  the  mouth,  on  an  average, 
a  little  less  acid  than  that  of  highly  susceptible  persons.     The 


316  DENTAL   PATHOLOGY 

difference  is,  however,  not  constant,  and  is  not  sufficiently  marked 
to  account  for  the  marked  difference  of  susceptibility."1 

This  conclusion  has  been  corroborated  by  Bunting,  who  like- 
wise found  very  little  difference  in  the  amounts  of  acids  formed 
in  the  saliva  of  immunes  versus  that  of  susceptibles.  Bunting 
expresses  his  conclusion  by  stating  that  the  ability  to  ferment 
carbohydrates  varies  in  different  individuals,  as  well  as  in  the 
same  individual,  but  that  this  rate  of  fermentation  bears  no  ap- 
parent relation  to  the  caries  susceptibility.9 

The  observations  of  Miller  have  been  confirmed  by  Lothrop  un- 
der the  direction  of  Gies,  the  distinguished  biological  chemist 
of  Columbia  University.  "The  results  obtained,"  says  Lothrop, 
"show  that  there  is  acid  production  regardless  of  the  condition 
of  the  mouth  and  teeth  of  the  individual  from  whom  the  cul- 
ture was  obtained."  Further,  as  to  whether  the  bacteria  from 
susceptible  mouths  ean  extract  more  lime  salts  from  the  tooth 
than  the  bacteria  from  immune  mouths,  has  also  been  the  sub- 
ject of  his  investigation,  and  he  has  found  that  cultures  of  bac- 
teria from  a  case  of  perfect  immunity  extracted  practically  as 
much  calcium  as  any  culture  from  decay  cases.10 

The  quantity  of  the  saliva  undoubtedly  plays  an  important  role. 
People  with  scanty  saliva,  almost  dry  mouths,  and  dry  mouths, 
are  more  susceptible  to  the  ravages  of  caries.  This  is  probably 
due  to  the  fact  that  in  the  presence  of  a  scanty  saliva  the  sur- 
faces of  the  teeth  are  not  freed  of  sticky,  starchy  deposits  and 
in  superficial  cavities  the  amount  of  saliva  is  not  sufficient  to 
dilute  the  acid  products  of  fermentation,  which  remain  in  a  con- 
centrated form,  more  rapidly  dissolving  the  enamel.  In  more  or 
less  dry  mouths  food  collects  upon  the  surfaces  of  the  teeth. 
and  particularly  in  the  interproximal  spaces,  remains  undisturbed, 
undergoes  fermentation,  and  soon  the  lactic  acid  end  product  dis- 
solves the  enamel. 

But  again,  viscosity  of  the  saliva,  viz..  whether  it  is  watery  or 
thick  and  sticky,  does  not  seem  to  correspond  in  a  constant  way 
with  susceptibility  to,  or  immunity  from,  caries.  A  thick  saliva 
has  been  found  in  mouths  free  from  caries,  and  a  thin  secretion 


sMiller,   W.   D.:     Dental    Cosmos,   xlv,   689. 

"Bunting:      Bulletin   ot    the   National   Dental   Association,    October,    1914. 
luLothrop,  Alfred  P  :     The  Oral  Microorganisms:     A  Bacterio-Chemical  study  of  Den- 
tal   Caries,   Journal   of   the   Allied   Dental    Societies. 


DENTAL    CARIES  317 

in  mouths  in  which  caries  was  rampant,  although,  in  the  majority 
of  instances  in  months  in  which  the  teeth  are  being  rapidly  disinte- 
grated through  caries  the  saliva  is  thick  and  ropy,  and,  vice 
versa,  a  thin  and  watery  saliva  is  secreted  in  moid  lis  not  so  sus- 
ceptible to  caries. 

Michaels  found  in  the  saliva  a  carbohydrate  which  he  supposed 
to  be  glycogen,  and  supposed  that  the  saliva  of  many  individuals 
susceptible  to  dental  caries  contained  such  a  carbohydrate.  This 
view  was  controverted  by  Miller,  although  he  was  inclined  to  be- 
lieve that  an  acid  fermentation  of  mucin  is  a  possibility,  and  per- 
haps is  accountable  for  the  development  of  cervical  caries.  In 
recent  years  Gies,11  after  an  exhaustive  investigation  into  the 
composition  of  the  saliva  in  its  relation  to  the  development  of 
caries,  has  shown  that  the  assumption  that  saliva  may  contain 
glycogen  in  sufficient  amounts  to  become  a  factor  in  the  produc- 
tion of  caries  is  not  supported  by  scientific  evidence.  But,  on 
the  other  hand,  his  experiments  with  mucin,  as  carried  out  with 
the  collaboration  of  Loewe,  indicate  that  this  glucoprotein  dis- 
solves calcium  from  the  tribasic  calcium  phosphate,  and  that 
it  is  highly  probable  that  mucin  is  able  to  dissolve  calcium  from 
enamel. 

The  foregoing  considerations  are  intended  for  the  purpose  of 
preparing  the  reader  for  a  discussion  of  the  predisposing  causes 
of  dental  caries. 

Predisposing-  Causes 

There  are  those  conditions  of  the  individual  teeth  or  of  their 
environment  which  favor  the  development  of  caries.  The  predis- 
posing causes  are  separate  and  independent  from  the  exciting 
causes  and,  contrary  to  the  latter,  are  not  entirely  external  to 
the  tooth.  Hence,  it  is  that  hypoplastic  defects  of  the  enamel, 
either  macroscopic  or  microscopic,  and  of  the  dentin;  the  amount 
and  composition  of  the  saliva;  the  position  of  the  teeth  in  the  arch; 
the  overlapping  of  the  teeth  or  having  broad  contacts;  the  diet 
as  ivell  as  the  age;  the  character  of  the  bacterial  flora;  and  the 
proper  hygiene  of  the  mouth  and  teeth — these  are  some  of  the  fac- 
tors which  may  influence  the  development  and  progress  of  caries. 


"Gies,    William   J.:      Biochemical    Studies    of    Saliva   and   Teeth,   Journal   of   the   Allied 
Dental    Societies,    1914. 


!18 


DENTAL   PATHOLOGY 


Hypoplastic  enamel  defects  predispose  to  caries  in  two  ways: 
(1)  by  affording  places  of  retention  for  food  debris;  and  (2) 
by  presenting  areas  of  tissue  lacking  in  normal  protectiveness 
by  reason  of  the  absence  or  defectiveness  of  the  interprismatic 
substance    and    of    the    enamel,    or    again   by   presenting    areas 


Fig.  237. — Defective  fissure  in  a  molar.  The  dark  area  from  a  lo  a  represents  imperfect 
calcification.  There  were  no  external  evidences  of  dental  caries,  although  at  b,  decal- 
cification has  started.  There  is  lack  of  interprismatic  substance  in  the  dark  area  as  well 
as  between  the  enamel  rods  beyond  the  dark  area.  Probably  as  high  a  proportion  as 
80  per  cent  of  the  fissures  of  permanent  molars  and  bicuspids  are  defective.  Invariably 
Nature's  effort  to  close  the  fissure  is  accomplished  by  depositing  an  amorphous  calcific 
mass  in  the  bottom  of  the  fissure.  In  this  mass  enamel  rods  are  sometimes  to  be  de- 
tected. 


of  decreased  enamel  thickness.  It  is  a  rarity  to  find  a  perfect  fis- 
sure in  the  molars  and  oicuspids,  for  surely  at  least  nine  out  of 
every  ten  molars  examined  clinically  and  microscopically  show 
plainly  these  defects  (Fig.  237).  No  break  may  exist  in  the  con- 
tinuity of  the  enamel  in  the  apex  of  the  fissure,  while  on  the  other 


DENTAL    CARIES 


319 


band,  these  fissures  may  be  so  deep  that  they  almost  reach  to  the 
dentin  at  the  dentoenamel  junction  and  afford  excellent  me- 
chanical retention  for  fermentable  food  particles.  In  such  loca- 
tions the  acid  end  produd  (lactic  acid)  remains  undisturbed  and 
undiluted,  and  caries  progresses  more  rapidly  than  in  other  loca- 
l  ions.  The  necessity  for  careful  and  frequent  supervision  of  these 
teeth  by  the  dentist  with  the  purpose  of  arresting  the  caries 
process  from  its  inception  or,  what  is  most  to  he  preferred,  of  pre- 
venting it  altogether,  can  not  he  too  strongly  emphasized  in  the 
minds  of  the  laity. 

But  defects  in  the  enamel  are  not  restricted  to  the  fissures  of 
bicuspids  and  molars,  nor  to  pits  in  the  lingual  surfaces  of  in- 
cisors, nor  to  irregularities  of  surface  in  any  of  the  aspects  of  a 
tooth.  Predisposing  causes  are  likewise  to  be  found  in  defects 
due  to  insufficiency  of  structure;  e.g.,  the  chalky  spots  or  those 
of  different  shades  of  brown,  which  are  the  result  of  the  partial 
or  almost  complete  absence  of  interprismatic  (binding)  substance 
with  a  low  grade  calcification  of  the  enamel  rods.  A  pit  on  the 
labial  surface  of  an  incisor  is  not,  however,  as  a  general  rule,  a 
location  of  choice  for  the  onset  of  caries,  for  the  reason  that 
the  enamel  rods  may  be  so  disposed  in  the  depression— in  a  mesh- 
like arrangement— as  to  offer  a  fair  degree  of  obstruction  to  the 
action  of  the  acid  end  product  of  carbohydrate  fermentation. 

Teeth  whose  dentin  has  an  abundance  of  interglobular  spaces 
are  predisposed  to  a  wide  spreading  of  caries.  Malposition  of 
one,  several,  or  of  all  the  teeth  in  the  arch  predisposes  to  caries 
by  favoring  the  lodgment  and  retention  of  fermentable  food  par- 
ticles. ''The  amount  of  foodstuffs,"  says  Bunting,  "which  are 
retained  about  the  teeth  is  in  direct  relation  to  the  character 
and  function  of  the  masticatory  apparatus.  In  case  the  dental 
arch  is  composed  of  well-formed  and  well-placed  teeth,  all  of 
which  are  in  good  occlusion  with  their  antagonists,  the  food  may 
be  finely  divided,  and  finding  no  favorable  place  for  lodgment, 
it  will  be  washed  out  of  the  mouth  and  swallowed.  Such  a  set  of 
teeth  may  be  said  to  be  'self-cleansing.'  On  the  other  hand, 
the  poorly  formed  teeth  and  teeth  which  are  irregularly  arranged 
and  in  abnormal  occlusion,  tend  to  offer  retention  for  foodstuffs, 
and  are  less  likely  to  be  self-cleansing.  In  the  regular  spaces 
between  such  teeth,  in  flat  interproximal  spaces,  and  in  wedge- 


320  DENTAL   PATHOLOGY 

or  V-shaped  areas  formed  by  the  overlapping  of  teeth,  food  will 
lie  wedged  and  retained  until  it  has  been  either  removed  me- 
chanically or  destroyed  by  bacterial   action." 

In  fact,  any  surface  of  any  tooth  which  is  inaccessible  to  the 
toothbrush  or  to  friction  during  mastication  is  a  favorite  place 
for  the  onset  of  caries.  The  bearing  of  the  diet  on  the  develop- 
ment of  caries,  as  has  already  been  indicated,  is  obvious.  The 
consumption  in  abundance  of  starchy  and  sweet  foods  is  a  strong 
predisposing  factor  of  caries;  and  vice  versa,  a  diet  poor  in 
these  carbohydrates,  but  consisting  of  meats  to  a  large  extent, 
is  conducive  to  restricted  caries.  Among  the  Gruachos  of  the  pam- 
pas of  Argentina,  who  subsist  mainly  on  meat,  caries  is  prac- 
tically absent,  while  among  the  aborigines  of  Chile,  where  the 
diet  is  mixed,  caries  is  present  in  a  relatively  large  proportion. 
The  Eskimos,  certain  meat-eating  tribes  of  North  American  In- 
dians. Icelanders,  and  Lapps,  are  almost  entirely  exempt  from 
caries.12 

Age  is  a  predisposing  factor  of  caries  to  the  extent  that  dur- 
ing the  early  years  of  life,  and  up  to  around  the  twentieth  year, 
the  greatest  susceptibility  to  dental  caries  exists  mainly  on  ac- 
count of  insufficient  mouth  hygiene  by  children  and  the  young, 
and  infrequent  examinations  by  the  dentist.  Pregnancy  is  proba- 
bly a  predisposing  factor  of  caries,  but  exclusively  by  virtue  of  the 
neglect  of  brushing  the  teeth  incident  to  the  woman's  general 
condition.  That  osteomalacia  of  pregnancy  affects  the  teeth  has 
never  been  proved;  but,  on  the  other  hand,  inflammations  of  the 
gingiva  and  gums,  which  occur  during  pregnancy,  again  by  rea- 
son of  neglect  of  the  toilet  of  the  mouth  and  teeth,  predispose 
to  caries  by  the  loosening  or  retraction  of  these  tissues  from  the 
neck  of  the  tooth  with  the  consequent  exposure  of  the  enamel 
near  and  at  the  neck  of  the  tooth  and  of  the  cementum  to  the  in- 
fluence of  carbohydrate  fermentation.  The  flabbiness  and  re- 
traction of  the  soft  tissues  around  the  necks  of  the  teeth  favor 
the  retention  of  food  particles. 

In  the  order  of  their  importance  the  predisposing  causes  were 
listed  by  ATiller  as  follows: 

1.  The  structure  of  the  teeth  [i.e..  poorly  developed,  soft,  porous 


'-.Miller,   \V.    D.:      Loc.   cit. 


DENTAL   CARIES  321 

teeth,  with  many  large   (dentinal)    [interglobular  spaces]    makes 
for  a  high  predisposition  to  caries. 

2.  Abnormally  deep  fissures  or  blind  holes  (foramina  ceca)  in 
molars  and  upper  lateral  incisors,  especially  in  cases  where  the 
enamel  also  is  poorly  developed. 

3.  Fissures  and  cracks  in  the  enamel. 

4.  Crowded  or  irregularly  placed  teeth. 

5.  Recession  or  loosening  of  the  gums. 

6.  Pregnancy. 

7.  Heredity. 

8.  Various  general  diseases  by  imparting  an  acid  reaction  to 
the  oral  secretions,  such  as  rheumatism,  gout,  diabetes,  gastro- 
enteritis, dyspepsia,  cancer  of  the  stomach,  scrofula,  rachitis,  and 
tuberculosis. 


CHAPTER  XX 
PATHOLOGIC  PROCESSES  IN  DENTAL  CARIES 

Dental  caries  is  a  molecular  disintegration  of  the  hard  tissues 
of  the  tooth  by  chemicoiacterial  agencies.  It  is  a  process  whose 
etiologic  factors  are  external  to  the  tooth,  and  which  consists 
of  two  distinct  steps  in  the  case  of  both  dentin  and  ceinentum: 
viz.,  (1)  the  disintegration  of  the  inorganic  matter  by  lactic 
acid,  the  result  of  carbohydrate  fermentation,  and  (2)  the  destruc- 
tion of  the  organic  matter  by  the  action  of  peptonizing  bacterial 
enzymes.  The  dissolution  of  the  enamel,  which  is  the  first  stage 
of  caries,  results  from  the  fermentation  of  carbohydrate  food 
by  the  direct  action  of  bacterial  enzymes.  The  enamel  con- 
taining only  a  minute  portion  of  organic  matter,  its  disintegra- 
tion occurs  exclusive  of  any  peptonizing  action.  The  enzymes  of 
mouth  bacteria  possess  the  property  of  splitting  monosaccharides 
into  lactic  acid.  The  starches  are  acted  upon  in  the  mouth  by  the 
amylolytic  enzyme,  ptyalin,  and  converted  into  maltose,  a  disac- 
charide.  The  starches  taken  into  the  mouth  as  food  have  the 
general  formula  (CGH10O'3)  x,  the  x  standing  for  an  unknown 
multiple.  The  action  is  one  of  hydrolysis,  and  may  be  expressed 
as  follows: 

Starch 

2C6H,„0-  -f  H20  +  ptyalin  —  C^BLO,,  (maltose). 

Cj.H^O,,  -)-  H,0  -\r  bacterial  enzyme=z  2C6H1206  (glucose,  or  dextrose). 

This  conversion  of  starch  into  maltose  takes  place  in  different 
steps: 

1.  Starch,  which  gives  a  blue  color  with  iodine. 

2.  Soluble  starch  or  amylodextrin,  which  gives  a  blue  color 
with  iodine. 

3.  Erythrodextrin,  which  gives  a  red  color  with  iodine. 

4.  a — Acroo  dextrin  (no  color  with  iodine). 

5.  /? — Acroo  dextrin  (no  color  with  iodine). 

•     6.  y — Acroo  dextrin,  and  possibly  other  dextrins. 
7.  Maltose. 

322 


l'ATI[()l,o<;i<     I'KOCESSES    IX    DENTAL    CARIES 


:;l':; 


Maltose,  C^ILJ ),,,  becomes  hydrolyxed  in  the  presence  of  one 
molecule  of  water  into  I  !12H24012  and,  bacterial  enzyme  being  avail- 
able, this  is  split  into  glucose  (dextrose)  2C6IT,J),.,  which  again,  in 
the  presence  of  a  bacterial  enzy ,  is  split  into  lactic  acid,  to  wi1  : 

2C6H1206  =  4C3H603  (lactic  acid). 

The  degrees  of  fermentation  of  certain  carbohydrates  by  bac- 
teria have  been  exhaustively  investigated  by  Gies  and  Kligler.1 

"Glucose  was  fermented  by  practically  all  the  strains  secured 
from  dental  deposits.  Lactose  and  sucrose  were  attacked  less 
regularly,  though  by  larger  majorities  of  these  strains.  The  bac- 
terial strains  tested  by  the  authors  in  this  series  of  investigations 
numbered  four  hundred  and  twenty-six.  The  accompanying 
table  embodies  the  result  of  these  investigations. 


SUGARS 
FERMENTED 


GLUCOSE       LACTOSE       SUCROSE 


GLUCOSE       GLUCOSE      GLUCOSE 
ONLY  ALSO  ALSO 

LACTOSE        SUCROSE 


GLUCOSE 
LACTOSE 

AND 
SUCROSE 
INDIVID- 
UALLY 


Number  of  bac- 
terial strains 
tested  426 

Percentage      of 
the   strains 
that  induced 
fermentation     99.5 


::si; 


326 


426 


15 


386 


'.26 


16 


322 


56 


"The  relative  fermentability  of  certain  sugars  in  equivalent 
volumes  by  typical  oral  bacteria,  as  measured  by  the  resultant 
amounts  of  acid,  has  also  been  determined  by  Gies  and  Kligler. 

"The  test  media  were  made  from  meat  infusions  according  to 
the  standard  methods  and  included  the  addition  of  one  per  cent 
of  the  sugar  to  be  tested.  The  titrations  were  made  with  N/20 
sodium  hydroxide  solution,  phenolphthalein  serving  as  the  in- 
dicator. The  results  as  expressed  in  the  following  table  are 
in  terms  of  the  number  of  cubic  centimeters  of  normal  hydroxide 
solution  necessary  to  neutralize  100  c.c.  of  the  culture  medium, 


1Chemical  Studies  of  the  Relations  of  Oral  Microorganisms  to  Dental  Caries,  Journal 
of  the  Allied  Dental  Societies,  December,  1915.  Because  of  the  scientific  value  of  these 
observations   they   are   quoted   in    full   with    the   consent   of   Professor   Gies. 


32-1  DENTAL    PATHOLOGY 

each  value  representing  average  acidity  produced  by  the  dif- 
ferent representatives  of  a  given  species  under  approximately 
equal  conditions  of  incubation  of  each  form : 


TYPE    OF 

ORGANISM 

GLUCOSE 

SUCROSE 

MALTOSE 

LACTOSE 

D.  rlavus 

2.5 

2.6 

2.7 

0.6 

Staphylococcus 

4.5 

2.5 

3.1 

4.5 

Streptococcus 

4.2 

4.2 

— 

4.0 

B.  acidophilus 

5.6 

0.9 

5.4 

5.8 

C.  placoides 

3.2 

4.3 

3.7 

0.5 

L.  buecalis 

3.9 

0.5 

2.7 

0.4 

Actinomyces 

1.9 

0.2 

0.4 

0.6 

"According  to  Kligler  the  recently  isolated  strains  of  staphy- 
lococci, streptococci,  and  bacillus  acidophilus,  represent  the 
most  active  acid-producers.  The  average  results  of  the  staphy- 
lococcus are  4.8,  streptococcus  4.8,  and  B.  acidophilus  7.0. 

"It  appears  from  the  foregoing  experiments  that  glucose  and 
maltose  are  more  rapidly  fermented  in  general  than  sucrose  and 
lactose,  also  thai  the  amounts  of  acids  produced  from  the  sugars 
used  were  fairly  constant  in  most  cases  for  each  type  of  bacteria. 
The  B.  acidophilus  is  capable  of  elaborating  and  withstanding  a 
greater  amount  of  acid  than  that  produced  and  resisted  by  any 
of  the  other  types." 

It  is  well  to  remember  in  connection  with  the  process  of  car- 
bohydrate fermentation,  as  bearing  upon  the  production  of 
dental  caries,  that  we  have  to  deal  with  monosaccharides  or  sim- 
ple sugars,  disaccharides  or  double  sugars,  and  polysaccharides 
or  multiple  sugars.  The  monosaccharides,  C^HjoO^.  are  directly 
split  by  bacteria  into  C3H(;03  (lactic  acid).  The  monosaccharides, 
or  hexoses.  are  the  sugars  found  in  fruits,  honey,  and  in  sugar 
of  milk  as  a  derivative  of  lactose.  These  are  glucose,  dextrose, 
and  grape  sugar,  levulose,  fructose,  and  galactose.  Dextrose,  lev- 
ulose  and  galactose  are  fermentable  by  yeasts  and  by  any  num- 
ber of  bacterial  enzymes  such  as  are  constantly  present  in  the 
mouth. 

Glucose  is  a  thick  syrup  obtained  from  corn  starch  by  the  ac- 
tion of  dilute  sulphuric  acid.  The  corn  starch  and  dilute  acid 
are  heated  together,  the  acid  first  converting  the  starch  into 
grape  sugar.     The  excess  of  acid  is  removed  by  treatment  with 


PATHOLOGIC    PROCI>>!>    IX    MENTAL    CARIES  325 

ehalk.     The  filtered  solution  is  either  evaporated  to  syrup  and 

sold  as  "glucose"  or  evaporated  to  dryness  and  sold  as  grape 
sugar  (Simon). 

Dextrose  is  found  in  honey.  Levulose  and  fructose  occur  in 
sweet  fruits  and  honey,  and  galactose  in  sugar  of  milk. 

The  disaccharides  or  saccharoses  comprise  principally  the  sug- 
ars obtained  from  cane  sugar  (saccharose),  from  beet  sugar  (sac- 
charose), and  from  milk  (lactose).  Their  general  formula  is 
CioHooO^.  In  the  process  of  hydrolysis  one  molecule  of  the  disac- 
eharide  takes  up  one  molecule  of  water  and  splits  into  two  mono- 
saccharide molecules,  thus  G1&s011  +  JI20  =  2CJlliOa.  To  the 
list  of  disaccharides  should  he  added  maltose  and  isomaltose — 
end  products  in  the  hydrolysis  of  starch. 

The  polysaccharides  are  starch,  glycogen,  dextrin,  inulin  and 
cellulose.  It  is  with  starch  that  we  are  distinctly  concerned  in 
the  study  of  dental  caries.  This  polysaccharide  is  insoluble  in 
cold  water,  alcohol,  and  ether.  It  conies  in  the  form  of  an  amor- 
phous, white,  tasteless  powder,  or  in  masses.  It  is  unabsorbable 
as  such,  but  must  first  be  hydrolyzed  into  maltose  and  then  into 
dextrose  through  the  action  of  an  organized  or  unorganized  en- 
zyme, in  either  case  the  intermediate  products  of  the  hydrolysis 
being  the  same.  Starch  is  widely  distributed  in  nature,  being 
found  in  the  seeds  of  cereals  and  leguminosa?.  and  in  the'  stems, 
roots  and  seeds  of  nearly  all  plants.  From  starch  down  to  the 
production  of  lactic  acid  the  chemical  reactions  involved  are  ex- 
pressed as  follows: 

STAECH  Maltose 

2CBH10O5  +  HX>  —  ptyalin  =  C^H^O,,.     . 

Maltose  Dextrose 

C^H^O^  +  H20  -f  maltase  enzyme  =  2C6H]2Oc. 

Dextrose  Lactic  Acid 

2C,.H1,01.  —  B.  enzyme  =  4C,H,.C\. 

The  dissolution  of  the  interprismatic  substance  or  of  the  enamel 
rods,  or  of  both,  is  followed  by  the  penetration  into  the  dentinal 
tubules  of  the  acid  end  product  of  fermentation  and  of  bac- 
teria which  have  the  power  of  dissolving  ( peptonizing)  the  or- 
ganic matrix  of  the  dentin.  As  the  enamel  is  penetrated  and  the 
decalcifying  agent  reaches  the  dentoenamel  junction  the  process 
spreads  laterally  with  a  rapidity  proportionate  to  the  prominence 


326  DENTAL   PATHOLOGY 

of  the  granular  layer.  The  more  marked  the  latter ;  i.e.,  the  greater 
the  size  of  the  expansions  into  which  the  tubules  open,  the  more 
rapid  and  greater  will  be  the  lateral  involvement  at  the  dento- 
enamel  junction. 

The  area  of  involvement  at  the  dentoenamel  junction,  because 
of  the  facility  with  which  bacteria  will  travel  along  this  line,  is 
greater  than  the  area  of  involvement  in  the  dentin  toward  the 
pulp.  It  is  for  this  reason  that  the  carious  process  in  the  dentin 
assumes  a  conical  shape  or,  as  expressed  by  Black,  the  tendency  is 
to  the  formation  of  a  conical  area  of  decay  with  the  point  of  the 
cone  toward  the  pulp  of  the  tooth  and  its  base  at  the  dentoenamel 
junction  (Fig.  238).    In  the  presence  of  wide  tubular  expansions 


Fig.  238. — Typical  conical  form  of  penetration  of  caries  into  the  dentin;  the  base  of 
the  cone  is  at  the  dentoenamel  junction  while  the  apex  of  the  cone  is  toward  the  pulp. 
(('..    V.    Black.) 

at  the  dentoenamel  junction — the  granular  layer — the  amount  of 
calcified  matter  to  be  acted  upon  by  lactic  acid  will  be  proportion- 
ately decreased,  so  that  caries  will  advance  rapidly  and  a  greater 
area  of  underlying  dentin  will  become  involved.  Caries  in  a  fis- 
sure, after  the  dentoenamel  junction  has  been  reached,  and  when 
an  excessive  granular  layer  is  present,  will  advance  more  quickly 
laterally  than  in  depth  into  the  dentin,  and  this  lateral  caries  will 
then  advance  toward  the  enamel  undermining  the  enamel  cap  over 
a  considerable  area. 

The  calcium  salts  of  the  dentin  are  dissolved  by  the  lactic  acid 
and  the  remaining  tough,  cartilaginous  matrix  is  then  acted  upon 
by  peptonizing  bacterial  enzymes.     The  bacteria  penetrate  the 


PATHOLOGIC    I'KooLSKKX    IN    DENTAL    CARIES 


327 


y 

if  v     '    ^    . 


Fig.    239. — Microorganisms   in    the   structure   of   the   dentin.    (Miller.) 


Fig.  240. — Microorganisms  in  the  structure  of  the  dentin.      (Miller.) 


328  DENTAL   PATHOLOGY 

dentinal  tubules  as  soon  as  access  to  them  is  secured  by  the  dis- 
solution of  the  overlying  enamel  (Figs.  239-242).  Here  they  can 
be  seen  in  considerable  numbers  and  occasionally  the  tubules  ap- 
pear distended,  evidently  as  the  result  of  the  action  of  the  or- 
ganisms upon  the  decalcified  or  quasidecalcified  structure  of  the 
tubules.  Black  was  of  the  opinion  that  microorganisms  do  not 
penetrate  into  the  dentinal  tubules  until  the  calcium  salts  have 
been  dissolved  for  a  short  distance  in  advance  of  the  bacteria. 

If,  now,  decalcification  should  proceed  in  an  external  direction 
from  the  dentoenamel  junction,  and  coincidentally  in  an  internal 
direction  into  the  dentin,  a  cavity  of  considerable  size  will  be 
formed  having  a  very  small  opening  externally.  The  lateral  prog- 
ress of  caries  at  the  dentoenamel  junction  is  designated  as 
lateral  caries,  and  the  progress  of  caries  from  the  lateral  involve- 
ment back  into  the  enamel  is  backward  curies.  The  tendency  for 
caries  to  spread  rapidly  as  above  described  is  not  the  case  in  all 
instances,  as  the  decalcification  of  the  enamel  and  dentin,  and 
liquefaction  of  the  organic  dentin  matrix,  may  be  a  slow  process 
from  the  beginning — a  long  time  elapsing  until  a  fair-sized  cavity 
is  formed.  The  involvement  of  the  dentin,  unless  proper  treat- 
ment by  filling  is  instituted,  will  continue  until  most  of  the 
crown  is  broken  down.  If  the  decay  advances  along  the  dento- 
enamel junction  and  from  there  several  paths  of  decalcification 
develop  into  the  enamel  and  the  dentin,  the  support  to  the  ename, 
rods  is  removed  and  these  will  soon  break  down,  the  top  of  the 
crown  will  collapse,  and  the  enamel  rods  will  be  washed  away 
by  the  saliva.  The  decay  advances  toward  the  pulp,  in  some  cases 
painful  symptoms  developing  as  the  result  of  pulp  irritation, 
while  in  others  no  painful  manifestations  occur  until  such  time 
as  it  is  too  late  to  save  the  pulp  or  even  the  tooth. 

The  formation  of  lactic  acid  in  the  deeper  structures  of  the 
dentin  is  explained  by  the  late  G.  Y.  Black  on  the  basis  of  os- 
mosis and  dialysis.  The  sugar,  as  it  is  formed  in  the  mouth  by 
the  fermentation  of  starches,  or  the  sugars  that  are  taken  into 
the  mouth  as  food  and  are  there  split  into  simple  sugars,  are 
dialyzed  into  the  deeper  structures  of  the  dentin.  Here  they  are 
further  split  into  lactic  acid  by  the  bacterial  enzymes  of  such 


PATHOLOGIC    PROCESSES    IV    DENTAL    CARIES 


329 


^?* 


V- 


."*** 


Fig.  241  — Microorganisms  in   the  structure  of  the  dentin.      (Miller.) 


Fig.    242. — Microorganisms    in    the    structure    of    the    dentin.       (Miller.) 


330  DENTAL  PATHOLOGY 

bacteria  as  have  previously  penetrated  into  the  tubules,  or  which 
are  in  the  deeper  layers  of  the  decalcified  dentin  matrix  in  prox- 
imity to  as  yet  sound  dentin.  By  the  same  process  of  dialysis 
the  inorganic  salts  of  the  dentin  which  combine  with  lactic  acid 
to  form  calcium  lactates  or  calcium  lactophosphates,  find  their  way 
into  the  saliva. 


CHAPTER  XXI 
CARIES  OF  THE  ENAMEL 

Etiology  and  Pathologic  Anatomy- 
It  develops  upon  the  enamel  in  spots  or  areas  which  favor  the 
attachment  of  bacteria  which,  as  the  result  of  their  activity  in 
a  carbohydrate  medium,  produce  lactic  acid.  This  dissolves  first 
the  interprismatic  substance  between  the  enamel  rods,  and  then 
the  rods  themselves.  This  incidence  is  easily  demonstrated  upon 
free  fragments  of  enamel  when  the  dissolution  of  the  inter- 
prismatic substance  by  lactic  acid  or  any  other  acid  brings  into 
view  the  outlines  of  the  individual  enamel  rods  by  establishing  a 
greater  margin  of  difference  between  the  refractiveness  of  the 
rods  and  that  of  the  interprismatic  substance,  the  rods  standing 
separated  from  each  other  at  their  free  ends  (Fig.  243). 

The  bacteria  which  induce  the  fermentation  of  carbohydrates 
upon  the  surface  of  the  enamel  are  supposed  to  become  collected 
under  a  protecting  gelatinous  mass  which  the  late  G.  V.  Black 
and  J.  Leon  Williams  have  considered  to  be  essential  in  the  de- 
velopment of  caries.  These  coatings  of  gelatinous  consistence, 
designated  by  Black  as  gelatinous  plaques,  were  by  him  inter- 
preted as  the  product  of  bacterial  activity.  The  slimy  deposits 
which  form  upon  the  surfaces  of  the  teeth,  particularly  during 
sleep  and  in  the  mouth  not  properly  cared  for,  are  not  the 
plaques  described  by  Black.  The  mucinous  plaque  is  not  the 
result  of  the  precipitation  of  mucin,  as  thought  by  many,  for 
the  reason  that  mucin  precipitates  in  the  form  of  flakes  which 
do  not  adhere  to  the  enamel.  The  formation  of  the  plaque  from 
mucin  is  a  purely  physical  process.  Black  considered  the  plaque 
as  an  essential  factor  in  the  retention  of  bacteria  upon  tooth  sur- 
faces and  also  in  the  localization  of  the  products  of  carbohydrate 
fermentation.  The  plaque  is  not,  however,  considered  by  Kirk1 
as  essential  in  the  progress  of  caries,  and  again,  Hopewell-Smith 


JKirk,    E.    C. :      A    Consideration    of    the    Question    of    Susceptibility    and    Immunity    to 
Dental  Caries,  Dental  Cosmos,  1910,  xli,  729. 

331 


332 


DENTAL   PATHOLOGY 


is  of  the  opinion  that  the  mysterious  plaque  is  nothing  more  than 
fragmentary  remains  of  Nasmyth's  membrane.  Gies  has  sug- 
gested the  use  of  weak  solutions  of  organic  acids  as  mouth  washes 
and  mouth  cleansers  on  the  assumption  that  the  precipitation  of 
mucin  in  flakes,  and  their  consequent  elimination  in  the  saliva, 
would  prevent  the  formation  of  the  mucinous  plaque.  Bunting  tells 
us  that  the  plaques  and  films  which  form  upon  the  teeth  are  not 
of  the  same  character  in  their  composition.     He  says  that  some 


Fig.    243. — Artificial   decalcification    of   the   enamel   by    one    per   cent    hydrochloric   acid    sim- 
ulating caries,      a.    dentin;    b,   sound   enamel;    c,   artificially   decalcified   enamel. 


forms  of  plaque  which  occur  in  certain  mouths  have  the  property 
of  favoring  caries  and  making  it  possible,  while  in  other  cases 
films  are  formed  which  are  protective  in  their  nature  and  which 
do  not  favor  acid  fermentation  in  their  substance. 

The  disappearance  of  the  cementing  substance  leads  to  the 
falling  and  washing  away  of  the  enamel  rods  (Fig.  244).  The 
first  symptom  of  caries  of  the  enamel  is  a  whitened  spot  pro- 


CARIES    OF    THE    ENAMEL 


333 


Fig.  244.— Caries  of  enamel  at  the  deepest  portion  of  the  cavity.  In  the  dentin  the 
lightest  area  at  a,  is  the  transparent  zone  of  Tomes.  At  b,  in  the  transparent  zone 
tubular  calcification  had  not  been  so  marked.  A  wall  of  enamel  at  c,  surrounds  the 
cavity  shown  at  d;  a  mass  of  decalcified  broken-down  enamel  is  shown  at  e    f    g    and  h 


334  DENTAL   PATHOLOGY 

duced  by  the  dissolution  of  the  cementing  substance.  Here  the 
enamel  feels  chalky  and  soft  to  the  explorer.  Localization  of 
caries  of  the  enamel  is,  in  the  order  of  frequency,  in  the  follow- 
ing areas  of  the  tooth:2 

1.  (a)   Pits  or  fissures  in  the  occlusal  surfaces  of  bicuspids  and 

molars. 

(b)  In  the  buccal  surfaces  of  molars. 

(c)  In  the  lingual  surfaces  of  molars. 

(d)  Occasionally  the  lingual  surfaces  of  the  upper  incisors. 

2.  In  the  proximal  surfaces  of  all  the  teeth. 

3.  In  the  gingival  third  of  the  buccal  or  labial  surfaces  of  all 

the  teeth,  and  rarely  in  the  lingual  surfaces. 

Certain  discolorations  upon  the  approximal  surfaces  of  molars 
and  bicuspids  are  probably  the  result  of  the  penetration  of  a 
slightly  decalcified  enamel  by  extraneous  substance  from  the 
saliva.  The  discolorations  in  fissures  of  bicuspids  and  molars  is 
attributed  by  Hopewell-Smith  to  color  changes  in  a  persisting 
Nasmyth's  membrane  by  certain  microorganisms,  to  wit:  B. 
fluorescens  liquefaciens. 

In  occlusal  surfaces  caries  develops  in  fissures  and  pits  because 
here  the  friction  of  mastication  is  unable  to  keep  these  locations 
clean.  Once  food  debris  becomes  lodged  in  a  pit  or  fissure,  it  un- 
dergoes fermentation,  with  the  result  that  the  interprismatic  sub- 
stance and  rods  are  dissolved.  The  occlusal  surfaces  are  sub- 
jected to  considerable  friction  during  mastication.  The  lingual 
surfaces  of  the  upper  and  lower  teeth  are  kept  clean  by  the  fric- 
tion  of  the  tongue,  and  the  buccal  surfaces  are  likewise  main- 
tained in  a  relative  degree  of  cleanliness  by  the  friction  of  the 
cheeks  and  lips.  As  a  general  proposition  it  may  be  said  that  the 
beginning  of  caries  is  located  in  areas  which  are  not  ordinarily 
subjected  to  friction,  either  by  the  cheeks,  lips,  tongue  or  during 
mastication.  Seldom,  if  ever,  do  the  prominent  lines  of  a  tooth — 
those  which  are  frequently  cleaned  by  either  muscle  friction,  the 
toothbrush,  or  the  food  itself  during  mastication — become  the 
original  seat  of  caries.  Rather,  it  is  the  points  on  the  surfaces  of 
teeth  that  offer  a  place  of  concealment  for  food  or  bacteria  that 
are  first  attacked  in  caries.    The  process  of  caries  is  limited  by  the 


2Black,   G.   V.:      Pathology   of   the   Hard  Tissues    of   the   Tooth,   vol.    i. 


CARIES  OF   Tin:    i;\a.mi.i, 


335 


position  of  normal  gum  (issue,  by  friction  in  mastication,  by  mus- 
cle friction,  and  by  artificial  cleaning. 


Fig.  245. — Caries  of  enamel  in  proximal  surfaces.  It  has  progressed  in  the  direction 
of  the  enamel  rods.  All  of  the  dark  area  (marked  X)  is  carious  enamel,  the  decalcifica- 
tion having  affected  the  interprismatic  substance,  which  is  practically  dissolved  away, 
the  individual  rods  can  be  distinguished  without  difficulty.  The  area  marked  E  is  sound 
enamel.  In  this  specimen  caries  bad  progressed  part  way  through  the  enamel.  (G.  V. 
Black.) 


In  the  approximal  surface  caries  of  the  enamel  exhibits  a  tend- 
ency to  follow  the  lengths  of  the  enamel  rods,  but  this  is  by 
no  means  a  constant  tendency.     Many  a  microscopic  section  re- 


ddb  DENTAL    PATHOLOGY 

veals  the  fact  that  caries  is  likely  to   progress  across  the  long 

axis  of  the  rods  after  a  certain  area  of  enamel  has  become  de- 
calcified (Figs.  245  and  246).  In  pits,  also,  the  progress  is  oc- 
casionally across  the  lengths  of  the  rods  (Fig.  247). 

The  pit  may  not  show  externally  any  evidence  of  caries,  but 
upon  examination  t lie  explorer  will  detect  an  opening,  and  caries 


Fig.    246. — Caries    of    enamel    in    a   proximal    surface    in    which    caries    has   made    c< 
erable    progress.      D,    dentin,    E,    enamel    (sound),    X,    carious    enamel,    the    dentoenamel 
junction   is   seen   between   D   and  B.      (G.    V.    Black.,) 

will  be  found  to  have  penetrated  the  thickness  of  the  enamel 
and  to  have  spread  across  the  lengths  of  the  enamel  rods  toward 
the  dentoenamel  junction. 

In  proximal  surfaces  the  predisposing  cause  of  caries  is  to  be 
found  in  the  failure  of  the  septal  tissues  to  completely  fill  the 
interproximal   space.      Under   normal   conditions    the    septal   tis- 


CARIES   OF   THE    EN  \  \li:i. 


337 


sues  will  fill  this  almost  to  tin atacl  point,  and  the  food  glides 

over  them  so  that  none,  or  only  very  small  particles,  becomes 
lodged  under  them.  Under  conditions  which  bring  about  inflam- 
matory disturbances  of  the  septal  tissues,  causing  them  to  recede, 
food  becomes  lodged  in  the  spaces  and  caries  begins  there,  be- 
cause that  portion  of  the  enamel  which  was  previously  protected 
is  now  exposed  to  the  influence  of  carbohydrate  fermentation. 

In  pits  and  fissures  caries  advances  frequently  across  the 
lengths  of  the  enamel  rods.  The  outline  of  the  caries  process  in 
these  localities  is  more  or  less  conical,  with  the  apex  of  the  cone 


Fig.  247. — Caries  of  enamel  in  a  pit.  The  whiteness  in  the  enamel  around  the  pit 
is  caused  by  the  dissolution  of  the  interprismatic  substance.  Caries  has  advanced  across 
the    long   diameter   of    the    enamel    rods.      (G.    V.    Black.) 


at  the  bottom  of  the  pit  or  fissure,  and  the  base  at  the  dento- 
enamel  junction  (Figs.  248  and  249).  In  these  cases  it  is  not 
unusual  to  find  the  enamel  thoroughly  undermined,  with  the 
opening  into  such  a  cavity  very  minute.  Food  which  accumu- 
lates in  a  pit  or  fissure  is  not  readily  disturbed,  so  that  any 
acid  produced  there  by  the  fermentation  of  carbohydrates  has 
ample  time  to  dissolve  the  rods  even  before  the  dentin  has  been 
penetrated,  because  it  remains  slightly  diluted,  being  not  readily 
washed  away  by  the  saliva. 

A  strong  predisposing  cause  of  caries  in  the  approximal  surfaces 
of  incisors  is  to  be  found  in  an  inflammation  of  the  septal  tis- 
sues.    Their  natural  rounded  form  is  destroyed,   or  the  tissue 


338 


DENTAL   PATHOLOGY 


shrinks  from  its  normal  position, — in  either  event  producing  a 
space  between  the  septal  tissues  and  the  approximal  surfaces  of 
the  teeth  in  which  food  accumulates  and  undergoes  fermentation. 
The  incidence  of  caries  here  is  usually  in  a  very  small  spot,  the 
whitened  surface  of  the  enamel  marking  the  location  at  which 


Fig.  J48. — Progress  of  enamel  caries  in  a  molar.  The  dark  area  represents  the  portion 
of  the  enamel  that  has  been  decalcified  by  the  lactic  acid  end-product  of  carbohydrate 
fermentation,  a,  dentin;  b,  b,  dentoenamel  junction;  c,  partly  decalcified  enamel;  d,  com- 
pletely decalcified  enamel,  c,  sound  enamel;  /,  interior  of  cavity. 

the  cementing  substance  has  been  dissolved  away.  Then  the 
advance  of  caries  is  exactly  the  reverse  of  what  occurs  in  pits 
or  fissures;  that  is  to  say,  the  penetration  is  in  the  shape  of  a 
cone  with  the  base  on  the  surface  and  the  apex  toward  the  dento- 
enamel junction.     The   central  portion  of  the   cone  is  in  close 


CARIES    OF    THE    ENAMEL 


339 


proximity  to  the  dentin,  and  it   is  there  that  the  dentin  is  first 
affected  by  the  acid  of  caries. 

The   tendency  in   the   approximal   surfaces   of   bicuspids   and 


Fig.    249. — 'Progress    of   enamel    caries    in    a    molar.      A    greater   enlargement    of    the    same 
section  shown  in  Fig.   247. 

molars  is  for  the  carious  process  to  begin  at  some  point  and 
spread  in  a  buccal  and  lingual  direction.  Spreading  toward  the 
occlusal  is  apparently  the  exception.3 


3Black,   G.   V.:      Operative  Dentistry,   i. 


CHAPTER  XXII 
CARIES  OF  DENTIN  AND  CEMENTUM 

Etiology  and  Pathologic  Anatomy 

Following  the   decalcification   of  enamel  by   the   acids  which 
result  from  the  fermentation  of  carbohydrates,  the   dentin  be- 


Fig.  250.— Caries  of  dentin  showing  decalcification  of  the  organic  constituents  and 
conversion  into  a  soft  cartilaginous  mass.  a.  pulp  chamber;  b,  b,  decalcified  dentin  which 
lias    been    converted    into    a   soft   cartilaginous    mass. 

comes  involved.  In  the  dentin  conditions  are  present  which  make 
for  a  difference  from  the  process  of  caries  in  the  enamel.  The 
decalcification  of  the  dentin— that  is  to  say,  its  conversion  into 

340 


CARIES   OF    DENTIN    AND    CEM1  \Ti    \l 


:;n 


a  tough  cartilaginous  substance — is  ■  designated  as  the  softening 
of  tli<'  dentin  (Figs.  250  and  251).  It  is  the  resull  of  the  dissolu- 
tion of  the   inorganic  salt    constituents   of  the   tissue.     This  soft 


b 


Fig.  251. — Caries  of  dentin  showing  decalcification  of  the  inorganic  constituents  anil 
conversion  into  a  soft  cartilaginous  mass;  a,  interior  of  cavity;  b,  decalcified  dentin 
which   has  been   converted   into   a   soft   cartilaginous   mass. 

mass  may  be  easily  peeled  off,  and  when  compressed,  discharges 
a  small  quantity  of  liquid  of  a  strong  acid  reaction   (Miller). 


342 


DENTAL   PATHOLOGY 


The  softening  of  the  dentin  is  followed  by  a  partial  or  complete 
liquefaction  of  the  organic  matrix.  This  organic  matrix  is  the 
cartilaginous  substance  which  remains  after  decalcification  has 
been  effected  and  which  upon  disintegration  or  liquefaction  leads 


Fig.    252. — Undermining    caries;    destruction    of    tooth    substance    from    within.       (W.    D. 

Miller.) 


to  the  formation  of  a  cavity.     Decayed  dentin  may  be  of  any 
shade  from  the  natural  color  to  black. 

The  progress  of  decay  in  dentin,  as  pointed  out  by  Miller,  fre- 
quently assumes  the  outline  of  a  Florence  flask  and  the  over- 
lying undermined  enamel  often  breaks  under  the  pressure  of  mas- 
tication.    In  microscopic  sections  the  enamel  is  seen  separated 


i  \\l;ii:s    OF    DKXTIX     VXD    CEMENTUM 


343 


from  the  underlying  dentin.  Caries  in  some  cases  proceeds 
rapidly  at  the  dentoenamel  line.  In  some  eases  the  caries 
process  advances  in  the  shape  of  a  narrow  canal  directly  to- 
ward the  pulp.  These  eases  are  designated  as  penetrating 
caries.  The  lateral  spreading  of  caries  in  the  dentin  at  the 
dentoenamel  junction,  or  the  progress  toward  the  pulp,  is 
governed  by  developmental  conditions.  In  fully  developed 
teeth,  with  many  interglobular  spaces  at  or  near  the  dentoenamel 


Fig.    253. — Undermining    caries;    destruction    of    tooth    substance    from    within. 

Miller.) 


(W.    D. 


junction,  the  decay  spreads  rapidly  on  all  sides  under  the  enamel ; 
when  teeth  are  dense  the  decay  travels  in  the  direction  of  the 
dentinal  tubules  toward  the  pulp.  In  some  cases,  in  the  molars 
and  bicuspids,  there  will  be  externally  a  relatively  slight  indica- 
tion of  caries  while  the  crown  of  the  tooth  may  be  thoroughly  un- 
dermined (Figs.  252.  253  and  254).  As  a  rule,  however,  as  the 
cavity  in  the  dentin  increases,  the  enamel  at  the  opening  becomes 
disintegrated   and   collapses  upon   the   slightest   pressure,   inas- 


344 


DENTAL    PATHOLOGY 


much  as  unsupported  enamel  easily  breaks  off.  The  progress  of 
caries  in  the  dentin  is  more  rapid  than  in  the  enamel.  The  pu- 
trefaction of  meats  in  a  cavity  through  its  alkaline  end  products 
may  lead  to  the  neutralization  of  the  acids  of  fermentation,  with 
the  arrest  of  caries,  but  the  caries  may  begin  anew  should 
starches  or  sugars  replace  the  putrefactive  material. 

The  two  phenomena  which  must  be  considered   in  connection 


Fig.   254. — Undermining  caries  of  approximal   surface;    undecayed   enamel   cusp    (a)    about 
to  break  away.      (W.  D.  Miller.) 

with  dentin  caries  are   (1)    transparency,  and  (2)   pigmentation, 
or  discoloration  of  the  decayed  tissue. 

Transparent  Zone  or  Zone  of  Tomes 

In  carious  dentin  a  transparent  area  between  the  pulp  and  the 
limiting  line  of  the  decayed  portion  is  usually  to  be  seen  in  mi- 
croscopic sections,  but  not  always,  the  latter  condition  being 
probably  due  to  the  unfavorable  plane  in  which  some  sec- 
tions are   cut.     When  present,   this  phenomenon  is   designated 


CARIES   OF    DENTIN    AND    CEMENT!    M 


345 


as  the  diaphanous  halo,  or  the  transparent  zone  of  Tomes  (Fig. 
255).  This  area  of  transparency  is  present  in  the  dentin  which 
lias  not  as  yet  become  involved  in  the  carious  process  because  of 
the  preponderance  of  inorganic  salt  content,  as  compared  with  ordi- 
nary dentin  thereby  offering  greater  resistance  to  decalcifying 
agencies  (Fig.  256).  It  has  the  form  of  a  cone  with  the  apex  to- 
ward the  pulp,  the  axis  of  the  cone  following  the  direction  of  the 
tnbuli.    Miller  found  thai  the  cone  is  bounded  on  each  side  by  an 


Fig.    255. — Caries    of   dentin.      At   b   is   shown   the   decayed   area   while   at   o   is    shown   the 
transparent  zone  of  Tomes.    (W.   D.   Miller.) 

opaque  baud.  At  least  three  hundred  specimens  of  decayed  teeth, 
which  had  been  worn  down,  mounted  on  opposing  plates  were 
examined  by  him,  and  in  no  instance  was  any  transparency  found. 
Further,  this  phenomenon  is  not  exclusively  an  accompaniment 
of  caries.  It  is  observed  in  sound  teeth  which  have  been  worn 
off  by  abrasion  or  erosion,  and  in  senile  teeth  where  the  roots 
in  their  entirety  frequently  become  transparent.  Miller  observed 
the  transparency  in  the  teeth  of  old  dogs  which  had  undergone 


34G 


DENTAL   PATHOLOGY 


abrasion.  The  true  cause  of  this  transparency  has  not  yet  been 
definitely  established,  but  several  things  have  been  definitely 
proved,  namely,  first,  that  it  does  not  occur  in  devitalized  teeth 
undergoing  caries ;  second,  that  decalcification  has  not  taken  place 
in  the  transparent  area,  as  proved  by  differential  quantitative  chem- 
ical anatysis ;  third,  that  microscopic  examination  of  the  transparent 
zone  shows  an  increase  in  the  thickness  of  the  walls  of  the  den- 
tinal tubules  within  the  transparent  zone,  with  a  corresponding 


Fig.    256. — Transparent    zone    of    Tomes    in    dentin;    it    offers    greater    resistance    to    de- 
calcifying   agencies    than    normal    dentin.       (W.    D.    Miller.) 

decrease  in  the  size  of  the  dentinal  fibrillar ;  and  fourth,  that  chemical 
analysis  shows  a  greater  proportion  of  lime  salts  in  the  transparent 
area.  The  area  of  transparency  is  in  all  probability  due  to  an 
increase  in  lime  salts,  with  a  consequent  thickening  of  the  walls  of 
the  tubules  and  a  corresponding  decrease  in  their  diameter  which 
results  in  an  equalization  of  the  normally  different  indices  of 
refraction  of  the  tubules  and  of  the  calcified  dentin  matrix. 
The  transparent  zone  is  therefore  the  result   of  the  stimula- 


CARTES   OK   DENTIN    AND   CEMENTUM  347 

tion  of  the  odontoblastic  layer  o£  tlie  pulp,  for  the  odontoblasts 
preside  over  the  deposition  of  additional  lime  sails  in  the  walls 
of  the  tubules.  This  increase  in  the  amount  of  calcined  tissue 
protects  the  pulp  against  the  ravages  of  caries  by  rendering  less 
rapid  the  decalcification  process  and  by  establishing  a  barrier  to 
the  thermal  insults  to  the  pulp  which  follow  a  loss  of  enamel 
structure,  even  in  a  small  area. 

Pigmentation 

Every  degree  of  discoloration  of  the  dentin  may  be  observed 
from  the  normal  color  of  the  tissue  to  a  yellow,  yellowish  brown, 
dark  brown,  or  black.  The  first  appearance  of  decay  is  not 
characterized  by  any  visible  discoloration  neither  is  it  present 
in  acute  caries.  But  it  is  present  in  chronic,  slow-developing 
caries,  and  hence  it  may  be  said  that  the  intensity  of  discoloration 
is  in  inverse  ratio  to  the  length  of  time  of  the  involvement.  Dis- 
coloration of  the  dentin  is  not  exclusively  a  phenomenon  of  decay 
but  occurs  also  whenever  dentin  is  laid  bare.  Discoloration  in 
worn  off  teeth  is  frequently  the  case  in  both  smokers  and  non- 
smokers.  The  same  phenomenon  is  observed  in  the  teeth  of  dogs. 
That  the  discoloration  arises  from  without,  and  is  not  a  phenom- 
enon of  dentin  caries,  strictly  speaking,  is  the  prevailing  opinion 
among  investigators.  It  has  been  variously  explained  by  the  ac- 
tion of  acids  upon  dentin;  by  the  color-forming  power  of  bacteria; 
and  Black  has  explained  it  by  the  settling  of  coloring  matter  de- 
rived from  the  action  of  hydrogen  sulphide  upon  such  metallic 
elements  as  may  be  introduced  into  the  mouth.  Miller  attributes 
discoloration  to  the  action  of  microorganisms  upon  organic  mat- 
ter. W.  H.  0.  McGehee1  has  found  that  practically  all  the  color- 
ing agents  or  dyes  which  are  used  by  manufacturers  for  coloring 
dentifrices,  stain  tooth  structure.  This  investigator  was  able  to 
stain  enamel,  dentin  and  cementum  in  the  laboratory  with  a  ma- 
jority of  dentifrices  on  the  market.  Tooth  structure  was  likewise 
stained  in  the  course  of  his  laboratory  experiments  by  dentifrices 
which  did  not  contain  added  coloring  matter  or  dyes,  the  pig- 
mentation in  these  instances  being  due  to  the  ingredients  in  the 
dentifrices  which  possess  color.    The  stains  were  found  to  be  pene- 


^IcGehee,  W.   H.   O.:     Dental  Cosmos,  March,    1912. 


348 


DENTAL    PATHOLOGY 


trating,  and  not  to  be  affected  by  sunlight  or  continued  washing. 
Clinically  it  was  found  by  the  same  experimenter  that  vital  teeth 
in  the  mouth  are  occasionally  stained  by  the  use  of  colored  denti- 
frices. It  was  brought  out  that  nonvital  teeth  stain  much  more 
readily  than  vital  teeth,  and  that  "vital  and  nonvital  dentin  and 
cementum,  whenever  exposed,  readily  take  almost  any  stain 
with  which  they  come  in  contact,  as  they  are  found  discolored  in 
practically  every  instance  in  which  they  have  been  exposed  for 


Fig.  257. — Caries  of  enamel  and  dentin 
which  beginning  on  the  mesial  surface  has 
progressed  beyond  the  enamel-cementum 
junction  and  involved  the  cementum  and 
underlying  dentin. 


Fig.  258. — Caries  of  cementum  on  la- 
bial surface  of  abraded  upper  left  central 
incisor. 


any  length  of  time;"  and  further  that  "crachs  in  the  enamel, 
abraded  and  eroded  surfaces,  cavities  of  decay,  and  other  similar 
conditions,  offer  excellent  evidence  of  stains  of  every  character." 
McGehee  condemns  the  use  of  colored  dentifrices,  his  experi- 
ments having  shown  that  when  constantly  used  they  will  stain 
the  tooth  structure. 

In  connection  with  the  study  of  dentin  caries  it  should  be 
noted  that  the  average  diameter  of  a  dentinal  tubule  is  greater 
than  that  of  most  of  the  bacteria  found  in  the  mouth,  and  conse- 


CARIES   OF    DENTIN    AND    CEMENT1   M  3-49 

quently  it  must  be  inferred  that  bacteria  find  their  way  into  normal 
tubules,  regardless  of  any  previous  decalcification  of  their  walls. 

The  Decay  of  Cementum 

The  inorganic  portion  of  the  cementum  becomes  decalcified  by 

the  action  of  the  acid  end  product  of  fermentation,  and  this  is 
followed  by  the  Liquefaction  of  the  remaining  organic  matrix 
(Figs.  257  and  258).  It  occurs  when  the  peridental  membrane 
has  been  detached  from  the  cementum,  food  becoming  lodged  in 
the  pockets  so  formed.  The  invasion  occurs  along  Sharper's 
fibers. 


CHAPTER  XXIII 
HYPERCEMENTOSIS 

General  Considerations 

Hypercementosis,  hypertrophy  of  the  cementum  (or  dental  ex- 
ostosis, as  it  is  sometimes  erroneously  called)  is  an  increase  of 
cementum  substance  which  serves  no  physiologic  purpose.  It 
is  observed  in  the  teeth  of  the  young,  as  well  as  in  those  of  the 
adult,  and  while  it  may  not  cause  any  reflex  painful  symptoms,  it 


l'*ig.     259. — Hypercementosis     of     lower 
first   bicuspid   and   deflection   of   its   root. 


Fig.     2d0. — Hypercementosis     in     upper 
right  second  molar. 


may,  on  the  other  hand,  be  the  etiologic  factor  of  serious  nervous 
manifestations.  The  cementum  is  not  a  self -reproducing  tissue: 
it  is  built  upon  the  dentin  from  the  dentoenamel  junction  to  the 
apex  on  all  the  aspects  of  the  root  by  the  follicular  wall,  which  is 
also  the  source  of  the  alveolar  process  which  serves  to  retain  the 

350 


HYPERCEMENTOSIS 


351 


tooth.  The  follicular  sac  persists  throughout  the  life  of  the  tooth 
as  the  peridental  membrane,  the  latter  retaining  the  function  of 
building  or  tearing  down  cementum  when  normal  or  pathologic 
conditions  demand  it. 


Fig.    261. — Hypercemen- 
tosis   in   upper  bicuspid. 


Fig.  262. — Hypercemen- 
tosis  of  root  of  lower  mo- 
lar— the  two  roots  are 
united  by  a  band  of  ce- 
mentum. 


Fig.  263. — Hypercemen- 
tosis  involving  the  three 
roots  of  an  upper  molar. 


Fig.  264. — Hyperce- 
mentosis  involving  the 
apical  area  of  the  three 
roots  of  an  upper  molar. 


Fig.  265. — Excessive  hy- 
percementosis  in  a  lower 
molar. 


Fig.  266. — Excessive  hy- 
percementosis  in  a  molar 
which  rendered  its  removal 
difficult  and  entailed  the 
fracture  of  the  surrounding 
alveolar    process. 


Hypercementosis  may  affect  only  the  apical  portion  of  a  root  or 
roots  of  a  tooth  (Figs.  259-264)  ;  it  may  affect  practically  the 
entire  root  area  of  the  roots  of  a  molar  or  bicuspid   (Figs.  265- 


352  DENTAL   PATHOLOGY 

268);  or  on]}'  one  root  or  two  roots  of  a  triple-rooted  molar;  and 
it  may  be  localized  upon  some  portion  of  the  root  in  the  form  of 
a  nodule  (Fig.  269). 


Fig.    2o~. — Hypercementosis    involving    the    three    roots    of   an    upper    left    fust    molar. 


Fig.     26S. — Hypercementosis     of    the     posterior  Fig.    269. — Nodular    form    of    hy- 

root   of   the   lower   first   molar.  percementosis. 

Etiology  and  Pathologic  Anatomy 

A  tooth  root  which  is  the  seat  of  hypercementosis  has  a  peri- 
dental membrane  which  for  a  prolonged  period  of  time  has  been 
continuously  subjected  to  a  degree  of  irritation  not  strong  enough 
to  cause  degeneration  in  the  cells  of  the  peridental  membrane, 


HYPERCEMENTOSIS 


353 


and  yel  strong  enough  to  cause  a  productive  stimulation.  An  ir- 
ritation from  any  source  which  will  cause  unrecoverable  degener- 
ations of  the  cells  of  the  peridental  membrane  can  not  and  will 
not  result  in  hypertrophy  and  hyperplasia  of  the  cementum. 
Therefore  inasmuch  as  in  hypercementosis  there  does  occur  an 
increase  in  the  thickness  as  well  as  in  the  number  of  cementum 
lamellae,  we  are  led  to  consider  the  process  not  merely  as  an  hy- 
pertrophy, bul  as  a  combination  of  both  processes,  viz..  hypertro- 
phy  and    hyperplasia.      The    cause   of   hypercementosis  mav   be 


Fig.    270. — Resorption   of  dentin  and   obliteration   of   the   resorbed   area   by   cementum. 


mechanical,  as  for  instance  the  pressure  against  the  root  of  an 
adjoining  tooth  caused  by  the  efforts  at  eruption  of  an  impacted 
tooth:  tooth  movement  in  orthodontia  :  the  effect  of  pressure  upon 
the  roots  of  an  impacted  tooth  by  the  unyielding  character  of 
the  surrounding  osseous  structures:  the  presence  of  a  particle 
of  root  filling  beyond  the  apical  foramen  through  continued 
stimulation  of  the  peridental  membrane;  the  pernicious  thread- 
biting  habit :  the  stimulation  of  the  peridental  membrane  in- 
directly from  the  gingiva  by  the  rough  and  protruding  edges  of 
fillings,  or  by  salivary  or  subgingival  calculi:  or  undue  stress  of 
occlusion  upon  one  or  several  teeth  when  the  result  is  several 


354 


DENTAL   PATHOLOGY 


hypercementosed  teeth  in  the  same  mouth.  Hypercemen- 
tosis  is  also  observed  where  a  root  whose  peridental  membrane 
has  been  the  seat  of  a  chronic  inflammation  caused  by  very  mild 
infection  which  has  spread  from  the  pulp;  and  while  the  inflam- 
mation may  have  brought  about  the  destruction  of  a  limited  area 
of  peridental  membrane,  it  has  also  stimulated  the  eementoblasts 


Fig.  271. — Ilypercementosis  accompanied  by  dentin  resorption  and  filling  in  of  the 
resorbed  area  of  dentin  by  cementum.  a,  normal  dentin;  b,  c,  outline  of  observed  dentin 
area,  cementum  of  repair  containing  vast  numbers  of  lacuna  with  their  respective  canalic- 
uli    radiating  toward   the   peridental    membrane. 


in  the  adjacent  healthy  peridental  membrane.  In  those  cases  of 
hypercementosis  in  -which  the  hypercementosed  area  is  involved  in 
a  chronic  dentoalveolar  abscess,  the  hypertrophy  started  at  a  time 
when  the  infection  was  of  such  a  degree  of  mildness  as  to  act  as 
a  regenerative  factor — a  stimulus.  After  the  hypercementosed 
area  was  formed,  the  adjacent  peridental  membrane  became  the 


IIYl'KRCEMENTOSIS  355 

seal     of    destructive    changes    upon     the    infection's    acquiring 
greater  virulence.    It  is  thus  thai  we  account  for  a  hypercemen- 

tosed  apical  root  area  in  juxtaposition  to  a  chronic  dentoalveolar 
abscess  (dental  granuloma).    In  chronic  peridental  inflammation 

in  connection  with  pyorrhea  alveolaris,  hypercementosis  may 
develop  in  root  areas  even  beyond  those  from  over  which  the 
peridental  membrane  has  been  destroyed.  It  may  also  develop 
consequent  upon  the  removal  of  Hie  pulp  when  it  may  be  the 
result  of  frequent  and  often  needless  manipulations  with  root 
canal  instruments  beyond  the  apical  foramen,  or  as  the  result  of 
the  action  of  concentrated  chemical  disinfectants,  or  again  fol- 
lowing a  mild  infection  of  the  periapical  peridental  membrane. 
Anatomically,  hypercementosis  manifests  itself  by  an  increase 
in  the  number  and  size  of  cementum  lamellae  and  occasionally 
by  areas  of  dentin  absorption  next  to  the  cementum  with  the  sub- 
sequent tilling  thereof  by  cementum  (Figs.  270  and  271). 


CHAPTER  XXIV 

ABEASION  AND  EROSION 

The  results  of  abrasion  and  erosion,  which  differ  in  etiology, 
are  clinically  identical.  It  may  be  possible  to  distinguish  by  im- 
plication between  them,  but  not  exclusively  on  the  evidence 
afforded  by  an  eroded  tooth  surface  or  by  an  abraded  one.  By 
carefully  investigating  the  forces  of  occlusion,  both  normal  and 
pathologic ;  the  character  of  the  lateral  contact  of  one  tooth 
with  another;  the  use  of  tough  or  coarse  foods;  the  effect  of 
extraneous  forces  upon  the  teeth,  such  as  from  pipe  stems, 
the  toothbrush,  cigarette  holders,  thread-biting — a  differential 
diagnosis  between  the  two  processes  may  be  established.  But  not 
so  on  a  clinical  examination  of  the  tissues  themselves  regardless 
of  the  influences  of  environment.  Abrasion  is  a  purely  mechan- 
ical process;  but  erosion  is  either  a  purely  chemical  or  a  chemico- 
mechanical  process. 

Etiology  of  Abrasion 

In  abrasion  of  the  crowns  of  teeth  and,  under  certain  circum- 
stances, of  the  roots,  when  these  are  exposed,  portions  are  worn 
away  producing  surfaces  with  a  high  polish  over  which  the  end 
of  an  explorer  will  glide  smoothly,  resembling  no  other  lesion  of 
the  enamel  or  dentin  except  erosion  resulting  from  chemicome- 
chanical  action.  The  teeth  suffer  from  restricted  degrees  of 
abrasion  from  the  time  they  assume  their  respective  positions  in 
the  arch  and  begin  to  exercise  their  physiologic  functions  (Fig. 
272).  When  this  abrasion  is  the  result  of  the  forces  of  masti- 
cation and  occurs  in  teeth  in  more  or  less  normal  alignment,  and 
the  diet  does  not  habitually  contain  coarse  or  gritty  foods  in  ex- 
cessive amounts,  it  can  be  considered  as  a  physiologic  process.  It 
is  a  pathologic  process  when  it  results  from  the  continued  friction 
between  the  surfaces  of  opposing  teeth  in  malocclusion,  when  the 
result  of  undue  friction  by  the  toothbrush,  or  when  because  of  the 
use  of  gritty  tooth  powders,  or  masticatories  such  as  chewing 
gum  or  tobacco,  or  of  holding  pipe  or  cigarette  stems  between  the 

356 


ABRASION    and   erosion 


357 


teeth.  The  loss  of  the  posterior  teeth,  throwing  the  bulk  of  the 
force  of  mastication  upon  the  anterior  teeth,  will  in  time  bring 
about  marked  abrasion  or  wearing  away  of  the  occlusal  surfaces 
of  the  anterior  teeth. 

Pathologic  Anatomy  of  Abrasion 

The  shape  of  the  abraded  surfaces  will  depend  upon  the  posi- 
tion of  the  tooth  in  the  arch  and  the  direction  and  extent  of  the 
frictional  forces.  It  may  be  nothing  more  than  a  decrease  in  the 
vertical  diameter  of  an  incisor  with  the  formation  of  a  square 
area  as  the  result  (Figs.  273,  274,  and  275);  or  it  may  have  pro- 
gressed to  the  extent  of  a  complete  wearing  away  of  the  crown  of 


Fig.   272.— Abrasion— mechanical   wearing  away   of  the   cusps  of   a   lower   molar. 

the  tooth  and  a  portion  of  the  root  (Figs.  276-279).  Mechanical 
appliances,  such  as  lingual  bars,  clasps,  etc.,  are  frequently  the 
cause  of  abrasion.  Such  instances  are  seen  in  Figs.  280  and  281. 
Abrasions  which  resulted  from  abnormal  stress  of  occlusion  are 
seen  in  tin-  scries  from  Fig.  282-289.  Any  tooth  may  suffer  from 
abrasion  of  such  severity  as  to  result  in  the  disappearance  of  all 
of  its  crown  and  even  a  portion  of  its  root,  The  abraded  surface 
presents  a  highly  polished  appearance,  and,  regardless  of  the  ex- 
tent of  tooth  structure  lost,  the  pulp  does  not  become  exposed, 
since  a  constructive  and  protective  process  takes  place  simul- 


358 


DENTAL    TATIIOLOOY 


taneously  with  the  loss  of  tooth  structure.  Tubular  calcification 
and  secondary  dentin  are  going  on  constantly  in  teeth  which  are 
undergoing  abrasion,  and  even  in  those  extreme  cases  in  which  all 
of  the  crown  and  a  portion  of  the  root  have  been  worn  away  the 


Fig.  273. — A  series  of  incisors  which  have  suffered  from  slight  abrasion.  At  a  and  b 
the  dentin  has  been  exposed  consequent  upon  the  wasting  away  of  the  enamel.  labially 
and   lingually,   and   has  assumed  a  brownish   yellow   color. 


Pig.    274. — Abrasion   of   the   incisal    edges   of   two   upper   central   incisors;    brownish    dis- 
coloration  of  exposed  dentin. 

remnant  of  pulp  tissue  will  be  protected  by  secondary  dentin. 
The  pulp  may  also  become  the  seat  of  degenerative  changes,  the 
calcific  form  being  the  most  frequently  encountered. 


V.BH  ^.SION    AND    I  ROi  [ON 


359 


Etiology  of  Erosion 

It  had  been  assumed  that  erosion  was  a  purely  chemical  proc- 
ess until  the  Late  W.  D.  Miller,  after  years  of  painstaking  in- 
vestigations and  experiments  in  the  laboratory,  was  v/iablc  to 
produce  the  characteristic  erosion  facel  by  the  action  of  acid  sub- 
stances alone.  He  was  able,  however,  to  duplicate  in  the  labo- 
ratory the  typical  erosion  surface,  with  its  high  polish,  by  a  com- 


Fig.  275. — Photomicrograph  of  ground  section  of  one  of  the  abraded  teeth  shown  in 
Fig.  274.  a,  enamel;  b,  dentin;  c,  abraded  enamel  with  a  chip  broken  off  in  mounting,  on 
right  side   of  picture;    d,  abraded  and   discolored   dentin. 


bination  of  acid  and  mechanical  action  (Fig.  290).  He  therefore 
reached  the  conclusion  that  at  least  the  experimental  form  of 
erosion  was  not  entirely  the  result  of  chemical  action.  Any  acid 
which  is  capable  of  abstracting  calcium  salts  from  the  enamel  and 
dentin,  or  of  dissolving  the  interprismatic  substance,  may  be  con- 
cerned in  erosion ;  any  acid  or  acid  substance  which  is  sufficiently 
powerful  to  disintegrate  the  organic  basic  substance  of  the  dentin 


360 


DKXTAL    PATHOLOGY 


may   cause   wasting    (erosion)    with   a   minimum   of   mechanical 
action.1 

In  a  case  of  extensive  erosion  studied  by  Kirk2  lactic  acid  ap- 
peared to  be  the  cause  of  the  wearing  away  of  the  surfaces  of 
the  teeth ;  and  in  other  cases  studied  by  him  he  has  attributed 


Fig.  276. — Upper  right 
cuspid.  Practically  the  en- 
tire crown  has  wasted  away 
on  account  of  abrasion. 


Fig.  277. — Upper  cuspids  which  for  many  years  had 
been  the  seat  of  abrasion.  The  entire  crown  in  each 
case    wasted   away    without    exposing   the    pulp. 


the  cause  to  the  action  of  acid  sodium  phosphate  and  acid  calcium 
phosphate,  which  are  secreted  by  the  gingival  glands  as  the 
manifestation   of  a   nutritional   disorder.      This   nutritional   dis- 


'Miller,  W.  D.:     Experiments  and  Observations  on  the  Wasting  of  Food  Tissue,  Dental 
Cosmos,   xlix,   No.    2. 

'Kirk,  E).   C:     Items  of  Interest,  xxiv,   No.   7,  July,   1902,  p.   511. 


ABRASION     \\1>    EROSION  36] 

order  is  responsible  for  the  presence  in  the  blood  of  an  excess  of 
carbon  dioxide  which  changes  the  basic  sodium  and  calcium 
phosphates  into  their  respective  acid  --alts. 


Fig.  278.  Fig.  279.  Fig.  280. 

Fig.  278. — Abrasion  of  lower  third  molar.      Complete  wasting  away  of  the  crown. 

Fig.   279. — Abrasion  of  lower  third  molar.      Complete  wasting  away  of  the  crown. 

Fig.  280. —  Spiral-shaped  abrasion  in  upper  left  cuspid  caused  by  an  ill-fitting  clasp. 
The  wearing  down  of  the  hard  tissues  advanced  beyond  the  boundaries  of  the  pulp  cham- 
ber which  was  filled  with  secondary  dentin. 


Fig.    281. — A   series   of   abraded    lower   cuspids,    upon    their   lingual    aspects,    the    result    of 
continuous   friction    by   ill-fitting   clasps   and   lingual   bars. 

Kirk  states  that  in  those  disorders  which  are  classified  as  dis- 
eases of  sulfoxidation,  the  blood  is  loaded  with  an  excess  of  carbon 


362 


DENTAL   PATHOLOGY 


Fig.  282. — Abrasion  of 
upper  right  central  incisor, 
the  result  of  an  abnormal 
frictional  stress  consequent 
upon  malocclusion;  exposed 
and    discolored    dentin. 


Fig.  283. — Abrasion  of 
lingual  surface  of  upper 
left  cuspid  reaching  beyond 
the  pu'P  chamber;  second- 
ary dentin  was  deposited 
in  sufficient  amount  to  keep 
the  pulp  protected  from  ex- 
ternal   injury. 


Fig.  284. — Abrasion  of 
the  labial  surface  of  the 
lower    right    first    bicuspid. 


Fig.    285. 


-Cup-shaped   abrasion    in    lower   molars,   the   result    of  abnormal    frictional   stress 
consequent    upon    malocclusion. 


ABRASION    AND    EROSION 


363 


dioxide.    "The  excess  of  carbonic  acid  in  the  blood  is  to  a  certain 
extent  taken  care  of  in  the  excretory  cells  of  the  kidneys  by  the 


Fig.    286. — Cup-shaped    abrasion    in    lower    first    molar,    the    result    of    abnormal    frictional 
stress    consequent    upon    malocclusion. 


Fig.  287.— Cup- 

shaped  abrasion  in  a 
lower  molar,  the  re- 
sult _  of  abnormal 
frictional  stress  con- 
sequent upon  maloc- 
clusion. 


Fig.  288. — Cup-shaped  abrasion 
in  lower  molar,  the  result  of  ab- 
normal frictional  stress  conse- 
quent  upon    malocclusion. 


Fig.  289. — Abrasion  in 
a  deciduous  molar,  re- 
tained in  the  arch  long  af- 
ter the  normal  time  for 
its    exfoliation. 


mass  action  of  carbonic  acid  upon  the  sodium  phosphate  of  the 
blood,  thus: 

H2C03  +  Na2HP04  =  NaHC03  +  NaH2P04 


364 


DENTAL   PATHOLOGY 


The  acid  sodium  phosphate  is  separated  by  the  kidneys  and 
carried  off  in  the  urine,  the  sodium  bicarbonate  being  returned 
to  the  blood  plasma,  which  is  thus  made  to  retain  its  alkalinity. ' ' 


Fig.   290. — Action   of  acid   calcium   phosphate   in   conjunction  with   friction   during  two  and 
one-third  years.     (W.  D.  Miller.) 


Fig.   291. — Tubular   calcification   in   the   dentin.     This   phenomenon  is   found   in   connection 
with   caries,   erosion   or   abrasion.      (W.    D.    Miller.) 


In  the  event  of  the  carbonic  acid  being  produced  in  proportions 
greater  than  normal  the  conversion  of  the  basic  sodium  phos- 


ABRASION    AND    EROSION  365 

phate  into  the  acid  sodium  phosphate  also  lakes  place  in  the 
buccal  glands,  so  that  their  acid  exudate  erodes  the  surfaces  of 
the  teeth. 

Pathologic  Anatomy  of  Erosion 

The  eroded  surfaces  may  be  shallow,  irregular,  saucer-shaped,  or 
wedge-shaped.  The  eroded  area  lias  a  highly  polished  and  dense 
surface,   and   1  lie   process  may  involve    the   enamel,   the   dentin, 

and  in  some  instances  also  the  eementum.  The  eroded  surfaces 
are  usually  located  upon  the  labial  and  buccal  surfaces,  rarely 
upon  the  lingual.  They  are,  as  a  rule,  markedly  sensitive,  al- 
though again  a  thorough  tubular  calcification  (Fig.  291)  under  the 
eroded  area  may  cut  off  the  tubules  from  the  pulp,  rendering 
the  area  absolutely  insensitive.  ( lalcification  of  the  dentinal  tubules 
and  secondary  dentin  are  constant  accompaniments  of  erosion 
to  a  greater  or  less  extent,  and  there  may  also  occur  degenera- 
tive changes  in  the  dental  pulp  leading  to  atrophy. 


CHAPTER  XXV 

THE   SALIVA 
Normal  and  Pathologic  Considerations 

The  saliva  is  the  mixed  secretion  of  the  three  paired  salivary- 
glands — the  parotid,  sublingual  and  submaxillary — and  of  all  the 
small  alveolotubular  glands  of  the  mucous  membrane  of  the  floor 
of  the  mouth,  the  palate,  cheeks  and  inner  lining  of  the  lips. 

Amount:  Salivary  Stimulants  and  Depressants. — The  amount 
of  saliva  secreted  in  twenty-four  hours  is  variable  among  in- 
dividuals and  for  each  one  under  varying  conditions  of  diet,  ex- 
ercise, temperature,  habits,  etc.;  it  has  been  estimated  at  from 
500  to  1200  cubic  centimeters.  The  secretion  is  influenced  by 
direct  or  indirect  stimulation,  which  may  be  normal  or  pathologic. 
The  smell  of  a  meal  in  the  course  of  its  preparation  and  the 
noise  incident  thereto,  the  sight  of  a  succulent  dish,  the  mas- 
tication of  an  appetizing  morsel,  etc..  are  common  instances 
of  indirect  and  direct  stimulation.  On  the  other  hand,  the 
salivary  secretion  is  pathologically  stimulated  by  inflamma- 
tions of  the  mucous  membrane  of  the  mouth  (the  several  forms  of 
stomatitis),*  and  by  drugs  such  as  pilocarpine,  physostigniine, 
iodine  and  its  compounds,  mercury  and  its  compounds,  (which  are 
specific  sialogogues),  acting  by  direct  stimulation  of  the  secreting 
cells  of  the  glands.  All  acids,  ethereal  bodies,  pungent 
substances,  tobacco,  nauseants,  such  as  ipecacuanha,  tartar  emetic, 
are  reflex  sialogogues.  The}*  act  by  producing  reflex  dilatation 
of  the  glandular  vessels  through  their  action  on  the  lining  of  the 
mouth.1  In  certain  nervous  disorders,  as,  for  instance,  during 
epileptic  attacks,  the  salivary  secretion  is  abundant.  In  the 
course  of  dental  operations  secretion  of  saliva  is  in  some  individ- 
uals markedly  increased.  It  is  the  result  of  reflex  stimulation. 
via  the  mucous  membrane,  by  mechanical  contrivances  and  be- 
cause of  the  pressure  upon  the  parotid  glands  by  the  overlying 
tissues  in  the  act  of  forcibly   opening  the  mouth.      The  pres- 


*At  the  climax   of  an   infectious   inflammation   of   the  mucous   membrane  of   the   mouth 
(stomatitis),  the  salivary  secretion  may  be  decreased  rather  than  increased. 

1Preston,   C.   II.:      In   N.   G.    Bennett's   Science   and   Practice  of   Dental   Surgery. 

366 


THE   SALIVA 


367 


ence  in  the  mouth  of  ragged  teeth  and  of  carious  cavities  is  also 
a  source  of  reflex  stimulation  of  the  salivary  secretion.  In  dis- 
eases of  the  hypoacid  diathesis  characterized  by  lymphatic  en- 
largements, in  chronic  follicular  tonsillitis  and  tuberculosis  the 
flow  of  saliva  is  abundant.2 

Sialorrhea  or  an  excessive  flow  of  saliva,  may  be  an  accompani- 
ment of  toxemias  and  febrile  disturbances.3  Dryness  of  the 
mouth  (xerostomia),  however,  is  not  a  rare  occurrence  in  con- 
nection with  febrile  disturbances  of  some  standing.  Pain  in  the 
teeth  produces  an  increased  flow  of  saliva.  The  amount  secreted 
by  the  parotid  is  less  than  one-third  of  the  amount  secreted  by 
the  submaxillary  and  sublingual  together,  and  may  be  as  low 
as  one-twentieth  or  one-thirtieth.  Acid  substances  produce 
greater  secretion  than  sweet  substances.4 

Color 

While  saliva  may  be  colorless,  grayish  or  whitish,  Michaels  has 
observed  that  this  may  vary  in  certain  pathologic  states,  while  in 
others  its  normal  color  is  not  altered.  The  saliva  of  individuals 
of  the  hypoacid  diathesis  is  colorless ;  that  of  the  gouty  and  of 
diabetics  is  grayish.  On  standing  the  "saliva  assumes  secondary 
colorations"  which  are  caused  by  oxidations  and  ammoniacal  fer- 
mentations of  organic  substances  contained  in  the  saliva,  mainly 
biliary  elements.  The  following  table  after  Michaels  is  in  itself 
sufficiently  explanatory: 

Different  Colors  Assumed  by  Human   Saliva  Upon   Standing,  and  the 

Sources  Thereof 
Normal  Pigments 

Pigments  which  produce  it. 
Eiliverdin 


Color 
Greenish 
Yellowish 
Blackish  green 
Bluish 
Brownish 
Dark  brown 
Red 

Golden  yellow 
Black 


Abnormal  Pigments 


Biliflavin 

Biliprasin 

Bilieyanin 

Bilifuchsin 

Bilihumin 

Bilirubin 

Urobilin 
Melanin 


:Michaels,    J.    B.:     Siaolo-Semeiology   Transactions    Fourth    International    Dental    Con- 
gress,  St.   L,ouis.   1904. 

3Howe:      Dental   Cosmos,   January,    1911. 
4Pickerill:     Oral  sepsis. 


368  DENTAL   PATHOLOGY 

The  saliva,  after  it  is  poured  on  a  watchglass,  must  be  ex- 
amined with  an  oblique  light,  the  rays  striking  the  fluid  from 
above  downwards. 

The  color  assumed  by  the  saliva  on  standing  corresponds,  in 
Michaels'  opinion,  to  certain  pathologic  states.  Thus,  in  gouty 
eczema  the  saliva  assumes  a  greenish  color;  in  indicanuria,  a 
bluish  color;  in  chorea,  a  brownish  color;  in  rheumatism  and 
oxaluria,  a  golden  yellow  color ;  and  in  carcinoma,  a  blackish  color. 
Normal  saliva  is  a  semitransparent,  frothy  fluid  the  aspect  and 
consistence  of  which  varies  according  to  the  proportion  it  con- 
tains of  ptyaline,  glycogen,  mucin  and  inorganic  salts.  Michaels 
has  stated  that  the  saliva,  if  left  in  a  bottle  for  some  time,  suffers 
a  change  in  its  consistence.  In  salivas  containing  cholesterin 
there  is  formed,  after  the  specimen  stands  for  some  time,  a  thick, 
greasy,  cream-white  coating  which  floats  on  the  surface.  This 
characteristic  is  often  found  in  the  saliva  of  diabetics.  ''In  the 
normal  state  the  sediments  occur  in  small  amounts  and  are  whit- 
ish. In  those  suffering  hepatic  insufficiency,  the  sediment  ap- 
pears brownish ;  in  cancer  patients,  it  is  blackish.  The  sediment 
is  composed  of  epithelial  cells  and  fibrinous  substance,  and  in  a 
few  hours  falls  to  the  bottom  of  the  vessel."  (  Michaels.) 

Odor 

Regardless  of  the  odor  which  results  from  fermentation  proc- 
esses in  the  saliva,  or  lactic  and  butyric  fermentation  in  indi- 
viduals of  the  hypoacid  diathesis,  certain  peculiar  odors  are  char- 
acteristic of  certain  diseases.  And  so  it  is  that  Michaels  connects 
a  garlic-like  odor  with  phosphorous  poisoning,  an  ethereal  odor 
with  diabetes,  an  acetonic  odor  with  diabetes  and  alcoholism,  etc. 

Taste 

The  taste  of  the  saliva,  which  is  insipid  in  normal  individuals, 
is,  for  instance,  bitter  in  disorders  of  digestion  with  hepatic  in- 
sufficiency, sweet  in  diabetes,  salty  when  soluble  chlorides  are 
present  in  the  blood  in  excess  of  the  normal,  and  metallic  in 
chronic  poisoning  with  mercury,  copper  or  lead. 


THE   SALIVA 

Constituents  of  the  Saliva 

Organic 

(a)  Mucin. 

(b)  Ptyalin. 
Proteins. 

(d)  Potassium  sodium  and    ammonium   sulphocyanids. 

Inorganic 


369 


(a)  Salts  of  Calcium 

(b)  Salts  of  Potassium 

(c)  Salts  of  Sodium 


Calcium  phosphate. 
Calcium  carl  innate. 
I  Calcium  bicarbonate   (in   fresh  saliva). 

|  Potassium  chloride. 
}  Potassium  phosphate. 

Sodium  chloride. 

Sodium  phosphate. 

Sodium  carbonate. 

Sodium  bicarbonate   (in  fresh  saliva). 

(  Magnesium  phosphate. 
I  Magnesium  carbonate. 


(d)  Salts  of  Magnesium 

(e)  Salts  of  Ammonium        J  Ammonium   carbonate. 


S  I'M  MARY 

The  composition  of  the  saliva  may  be  summarized  as  follows: 
Water  994.90 

Organic  matter  3.60 

Inorganic    matter  1.50 

The  secretion  contains  epithelial  cells  which  have  been  thrown 
off  by  the  epithelium  of  the  mouth,  and  salivary  corpuscles  de- 
rived from  the  lymphoid  tissue  of  the  faucial,  lingual,  and  pharyn- 
geal tonsils;  but  these  have  no  relation  to  the  salivary  glands.  On 
entering  the  mouth  these  corpuscles  swell  and  their  protoplasm  be- 
comes granular. 

Mucin 

The  source  of  mucin  is  from  the  submaxillary  gland  and  the 
mucin  secretions  of  the  mucous  membrane.  It  is  precipitated  by 
weak  acid  solutions,  e.g.,  acetic  and  lactic  acids  and  by  acid  salts. 
It  is  the  probable  material  of  which  the  so-called  "plaques"  are 
composed,  but  not  as  the  result  of  chemical  precipitation.     It 


370  DENTAL   PATHOLOGY 

undergoes  alkaline  decomposition  through  the  action  of  mouth 
organisms,  and  may  be  regarded  under  certain  conditions  only 
as  an  agent  which  protects  the  enamel,5  for  Gies  has  shown  that 
the  result  of  the  fermentation  of  mucin  has  a  dissolving  power 
upon  tricalcium  phosphate.  But,  on  the  other  hand,  the  mucin 
is  not  deposited  by  itself  alone  on  the  surfaces  of  teeth.  Through 
its  viscosity  or  stickiness  it  binds  carbohydrate  material  to  the 
teeth  and  soft  tissues  and  the  bacteria  enmeshed  in  the  mass  bring 
about  the  fermentation  of  the  carbohydrate  material  with  the  ul- 
timate production  of  lactic  acid,  the  dissolving  agent  of  enamel 
interprismatic  substance  and  rods.  Consequently,  even  should  the 
mucin  undergo  putrefactive  decomposition  with  the  formation  of 
alkaline  end  products,  these  are  soon  neutralized  and  rendered 
valueless  as  protective  agents  in  the  presence  of  acid  substances 
when  in  amounts  sufficient  to  counteract  this  alkalinity  and  also 
to  dissolve  the  enamel  structure;  this,  because  the  proportion  of 
fermentable  material  exceeds  by  far  the  amount  of  the  mucin  in 
the  slimy  coatings  or  deposits. 

It  may  be  precipitated  not  only  by  weak  acids,  but  also  by  acid 
salts,  such  as  acid  potassium  tartrate,  and  acid  sodium  phosphate 
(Kirk).  Ropy  saliva,  in  which  this  "ropiness"  or  "stickiness" 
is  due  to  the  relatively  high  mucin  content,  is  associated  with 
progressive  caries  in  children  and  young  persons.  The  source 
of  mucin,  to  the  extent  of  80  per  cent  of  its  volume,  is  from  the 
mucous  membrane  mucin-secreting  glands,  and  the  proportion 
of  salivary  mucin  has  been  found  by  Vulpian  to  be  as  high  in 
one  healthy  man  as  0.32  per  cent. 

Ptyalin 

Ptyalin  is  an  anxiolytic  enzyme,  because  it  possesses  the 
property  of  transforming  complex  carbohydrates,  such  as  starch 
and  dextrin,  into  simpler  bodies.  When  the  amount  of  ptyalin 
is  inadequate,  the  digestion  of  starch  in  the  mouth  is  slow  and  the 
intermediate  products,  the  dextrins,  help  to  bind  the  starchy 
mass  to  the  teeth.  The  microorganisms  contained  in  the  mass 
cause  the  fermentation  of  the  enmeshed  carbohydrates,  with  the 


spickerill,   II.   1'.:     Prevention  of  Dental   Caries,   and   Oral   Sepsis,   S.    S.   White   Dental 
Mfg.   Co.,  Philadelphia,   1914. 


THE   SALIVA  371 

production  of  lactic  acid,  which  arrests  the  action  of  ptyalin  and 
decalcifies  the  enamel.6 

The  ptyalin  index  of  normal  resting  saliva  is  increased  more 
than  tenfold  by  acid  stimulation  (Pickerill).  The  transforma- 
tion of  starch  into  the  end  product  maltose  is  by  a  process  of 
hydrolysis,  effected  by  ptyalin,  the  intervening  products  being 
erythro-dextrin,  a-achroo-doxtrin,  /?-achroo-dextrin,  isomaltose 
and  finally,  maltose.  The  action  of  ptyalin  (salivary  amylase) 
is  arrested  in  the  presence  of  even  a  trace  of  free  acid,  as  weak  a 
solution  as  0.003  per  cent  having  that  effect.  It  acts  best  in  a 
neutral  or  slightly  alkaline  solution.  The  digestion  of  starch  by 
ptyalin  in  the  stomach  continues  for  about  forty  minutes  or 
longer  after  the  ingestion  of  food,  or  until  actual  contact  of  the 
arresting  free  hydrochloric  acid  with  the  ptyalin. 

Albumin 

Albumin  is  of  the  nature  of  globulin ;  it  is  precipitated  by  heat, 
and  is  found  in  very  small  amounts.  The  amount  increases  in 
Bright 's  disease  (Vnlpian,  Pouchet,  Michaels).  In  one  patient 
suffering  from  albuminuria  of  cardiac  origin  the  percentage  of 
albumin  in  the  saliva  was  0.145,  and  in  one  suffering  from  par- 
enchymatous nephritis  it  Avas  0.182  (Vulpian,  with  affirmative 
control  by  Pouchet).7 

The  Sulphocyanids  (Potassium,  Sodium  and  Ammonium) 
KCNS;  NaCNS;  NHtCNS 

Sulphocyanids  are  found  in  mixed  saliva  in  proportions  vary- 
ing from  0.0075  to  0.0100%..  The  proportion  seems  to  be  greater 
in  individuals  of  the  hyperacid  diathesis  than  in  those  of  the  hy- 
poacid.  Rheumatic  patients  exhibit  a  greater  amount  than  gouty 
patients,  but  in  patients  with  phosphaturia  the  amount  is  less 
than  in  gouty  patients.  The  complete  absence  of  sulphocyanids 
has  been  associated  with  gastrointestinal  disorders.  Prof.  Gies'8 
studies  lead  one  to  conclude  that  the  amount  of  sulphocyanids 
in  the  saliva  bear  no  relation  ivhat soever  to  the  incidence  or  prog- 
ress of  caries. 


"Pickerill:     Loc.  cit. 

7Michaels,  J.    P.:      Transactions   of   the   Fourth   International    Dental    Congress. 

8JournaI  of  the  Allied   Dental   Societies,    1911,  vi,   pp.   289,  297,   323,   and   334. 


372  DENTAL    PATHOLOGY 

Max  Kahn  likewise  reports  negative  findings.9  The  sulphocy- 
anids  in  the  saliva  are  products  of  protein  metabolism  and, 
Piekerill  helieves.  of  the  breaking  down  of  such  mouth  proteins 
as  mucin,  epithelium,  leucocytes,  etc.  He  adds  that  the  sul- 
phocyanids  in  the  saliva,  "may  have  a  beneficial  effect,  if  only 
present  in  sufficient  amount."  This  investigator  found  that  the 
sulphocyanids  could  exert  a  slight  antiseptic  action  if  present  in 
the  saliva  in  a  one  per  cent  solution  or  over.  But  as  the  percentage 
is  practically  always  constant  and  does  not  vary  by  the  application 
of  such  stimuli  as  cause  an  increase  in  the  percentage  of  other 
salivary  constituents,  the  role  of  the  sulphocyanids  as  a  preventive 
of  dental  caries  is  nil. 

The  amount  of  sulphocyanids  may.  however,  be  rapidly  in- 
creased in  man  by  the  administration  by  mouth  of  repeated  doses 
of  potassium  sulphocyanid  of  from  %  to  1  grain  in  water.  The 
percentage  in  the  saliva  was  increased  to  0.0200  from  0.0100  fa 
fair  average  of  sulphocyanid  content)  in  three  hours  follow- 
ing a  dose  of  0.1  gram  in  water.  This  increased  percentage  per- 
sisted for  seven  days.10 

Inorganic  Constituents 

The  inorganic  salts  are  alkali  and  earthy  phosphates,  carbon- 
ates, bicarbonates  and  chlorides.  The  alkali  group  includes 
potassium  and  sodium  phosphates;  sodium  carbonate  and  bicar- 
bonate (in  fresh  saliva);  ammonium  carbonate;  potassium  and 
sodium  chloride.  The  earthy  group  includes  calcium  phosphate, 
carbonate,  and  bicarbonate,  the  latter  in  fresh  specimens.  Mag- 
nesium, because  of  its  behavior  toward  analytic  re-agents,  is  left 
in  the  so-called  alkali  group  of  metals  (Simon).  It  is  found  in 
saliva  as  a  phosphate  and  carbonate.  The  phosphates  and  car- 
bonates may  exist  in  the  saliva  as  acid  or  alkaline  salts. 

In  the  gouty  diathesis  the  proportion  of  chlorides  is  increased, 
and  decreased  in  febrile  affections.  Ammonium  carbonate  is  ac- 
cording to  Michaels,  a  constant  constituent  of  the  saliva,  being 
present  in  comparatively  large  proportions  in  the  hyperacid  diath- 
esis (rheumatism,  gout). 


:'Dental  Cosmos,   1914,   lvi,    175. 
10Pickerill:     Loc.  cit. 


THE   SALIVA  373 

In  addition  to  all  of  the  foregoing  constanl  constituents  of  the 
saliva,  Michaels  records  the  pathologic  presence  of  fatty  phos- 
phorous compounds  (lecithin  and  tyrosin),  glycogen,  biliary 
pigments  and  biliary  acids"  urobilin,  cholesterin,  glucose,  so- 
dium and  ammonium  urates,  urea,  propionic  acid,  acetone,  suc- 
cinic acid,  etc.  The  presence  of  these  abnormal  constituents  is 
associated  with  certain  pathologic  slates.  Thus,  in  the  saliva  of 
individuals  of  the  hyperacid  diathesis  sodium  and  ammonium 
urates  have  been  found;  in  salivas  of  diabetics,  propionic  acid, 
glucose,  and  acetone;  and  in  that  of  cholemics  and  uremics,  bil- 
iary elements. 

Reaction 

The  old  time  custom  of  testing  the  reaction  of  the  saliva  by 
means  of  litmus  is  utterly  unreliable.  The  saliva  exhibits  an 
amphoteric  reaction  and  as  pointed  out  by  Kirk,  in  a  specimen  of 
saliva  the  acidity  is  not  due  to  an  uncombined  acid,  but  to  the 
presence  of  a  salt  which  has  resulted  from  only  the  partial  re- 
placement of  the  hydrogen  by  the  metal;  the  alkalinity  in  the 
same  specimen  is  due  to  the  presence  of  the  alkaline  salt  of  the 
acid  by  replacement  of  twice  the  number  of  hydrogen  atoms. 
Thus,  in  a  specimen  of  saliva  the  presence  of  the  acid  ion  of  the 
basic  salt  of  phosphoric  acid  may  cause  blue  litmus  to  turn  red 
and  the  basic  ion  may  cause  red  litmus  to  turn  blue,  if  the  salts 
do  not  neutralize  each  other. 

Phenolphthalein  is  the  indicator  most  commonly  employed. 
The  Scientific  Research  Committee  of  the  National  Dental  As- 
sociation has  recommended  that  it  be  used  as  an  indicator  and 
titration  be  made  against  NaOH.  Phenolphthalein  is,  however, 
sensitive  to  C02,  which  may  obscure  the  reaction  for  free  and 
uncombined  acids.  Bunting12  recommends  the  passing  of  C02- 
free  air  through  the  sample  to  be  tested,  while  heated  to  a  tem- 
perature not  over  50°  C.  All  uncombined  C02  will  be  discharged 
in  from  five  to  ten  minutes.  This  method  is  less  objectionable 
than  that  of  boiling  the  saliva.  Saliva,  the  mixed  secretion  of  the 
parotid,  submaxillary,  sublingual,  and  buccal  glands  is  alkaline  to 
litmus  although  the  same  specimen  may  be  amphoteric  to  litmus 


"Gorup-Besanez:       (Quoted   by    Michaels,   J.    P.,    loc.    cit.) 

"Bunting:     Official    Bulletin    of    the    National    Dental    Assn.,    October,    1914,    i,    No.    4, 
p.   38. 


374  DENTAL  PATHOLOGY 

owing  to  the  presence  of  acid  and  basic  phosphates  and  carbon- 
ates. Saliva  is  as  a  rule  acid  to  phenolphthalein  because  of  the 
presence  of  C02  and  acid  phosphates  and  carbonates;  it  usually 
is  alkaline  to  methyl  orange,  which  is  not  affected  by  C02.  All 
salivas  are  hence  alkaline  to  the  latter  indicator  and  to  lacmoid 
and  Congo  red.  The  amphoteric  behavior  of  the  saliva  is  due  to 
the  presence  in  the  fluid  of  free  H  and  OH-ions  and  the  reaction 
of  the  fluid  is  determined  by  the  predominance  of  either  of  these 
groups  of  free  ions.  The  saliva  from  a  resting  gland  differs  in 
reaction  from  that  flowing  under  a  stimulus.13  and  as  shown  by 
Piekerill  the  reaction  varies  according  to  the  nature  of  the  stimu- 
lus and  the  length  of  time  it  is  applied.  The  result  of  this  stimu- 
lation differs  in  different  individuals.  Thus  it  has  been  found 
by  this  investigator  that  the  alkalinity  is  increased  by  acid 
stimuli  which,  from  among  all  other  substances,  produce  the 
greatest  alkalinity  per  cubic  centimeter,  and  that  the  alkalinity 
is  depressed  by  such  articles  of  daily  food  as  white  and  brown 
bread,  with  or  without  butter,  and  cake,  biscuit,  meat  and  sweets. 
Pain  causes  a  very  alkaline  reaction.  The  average  alkalinity  of 
the  parotid  saliva  per  cubic  centimeter  is  greater  than  that  from 
the  other  glands;  but  as  the  rate  of  flow  from  this  gland  is  low. 
the  total  alkalinity  per  minute  is  very  much  less  (Piekerill). 

The  character  and  the  amount  of  normal  or  abnormal  constit- 
uents of  the  saliva  reflect  to  quite  an  extent  the  nature  of  the 
biochemical  reactions  in  the  body.  It  varies  in  composition  not 
only  in  different  individuals,  but  at  different  times  in  the  same 
individual,  because  of  the  temporary  or  constant  results  of 
nutritional  phenomena  and  of  bacterial  or  chemical  intoxications. 
The  investigations  of  Michaels,  Gies,  Kirk.  Piekerill,  Howe,  Bunt- 
ing, Ferris  and  others  have  made  it  possible  to  enlarge  our  knowl- 
edge of  saliva  and  of  its  possibilities  in  semeiology.  Howe,  for 
instance,  has  shown  that  an  excessive  carbohydrate  diet  is  mani- 
fested in  the  saliva  by  the  presence  of  imperfectly  oxidized 
bodies ;  that  in  artificially  induced  glycosuria  the  saliva  contains 
traces  of  glucose  or  an  aldehyde,  and,  in  intestinal  disturbances, 
traces  of  indiean.  Howe's  investigations  have  led  to  conclusions 
confirmatory  of  the  work  of  Michaels  and  Kirk:  that  the  saliva 
is  a  fair  barometer  of  normal  and  abnormal  body  reactions. 


"Howe,   Percy   R. :     Dental  Cosmos,  lv,   1913. 


CHAPTER  XXVI 

THE  GUMS  AND  GINGIVAE 
Normal  and  Pathologic  Considerations 

The  gums  are  the  soft  tissues  which  cover  the  alveolar  process 
of  the  maxilla  and  mandible  and  extend  from  the  crest  of  the 
alveolar  process  to  the  commissure  of  the  lips  and  cheeks  exter- 
nally; and  internally  arc  continued,  in  the  maxilla  with  the  pala- 
tal mucous  membrane,  and  in  the  mandible  with  the  mucous  mem- 
brane of  the  floor  of  the  mouth. 

The   gums   consist    of    an   underlying   fibrous    connective-tissue 
mat  containing  a  few  elastic  fibers,  and  of  an  external  covering  of 
stratified  squamous  epithelium  (Figs.  292,  293,  and  294).     The 
underlying  fibrous  connective-tissue  mat,  designated  as  the  tunica 
propria  or  the  stroma  of  the  mucous  membrane,  presents  a  number 
of  elevations,  or  papilla,  which  penetrate  into  the  epithelial  layer, 
giving  to  the  oral  mucous  membrane  an  appearance  under  the  mi- 
croscope sui  generis.    Connective-tissue  cells,  round,  stellate  and 
spindle-shaped,  are  supported  by  the  fibrous  tissue  of  the  tunica 
propria.     The  mucous  membrane  is  connected  with  the  underlying 
structure  by  means  of  a  layer  of  areolar  tissue,  i.e.,  the  submucous 
layer.      The    attachment    of   the   mucous   membrane   may,    under 
normal  conditions,  be  very  firm  as  in  the  case  of  the  gums  and  the 
mucous  membrane  covering  the  hard  palate,  or  very  loose,  as  in 
the  case  of  the  buccal  and  labial  mucous  membrane  and  that  form- 
ing the  lining  of  the  floor  of  the  mouth.     The  blood  supply  of  the 
gums  is  very  rich,  being  distributed  to  the  connective-tissue  under- 
structure  (stroma)  the  epithelial  covering  obtaining  its  nutrition 
by  osmosis  from  the  capillary  loops  at  the  apices  of  the  papilhe. 
The  arteries  after  penetrating  and  passing  through  the  submucous 
areolar  tissue,  break  up  into  arterioles,  which  in  turn  break  up 
into  capillary  loops  in  the  substance  of  the  papillae  in  close  rela- 
tion with  the  epithelial  layer.     The  veins  follow  the  arteries  in 
their  general  course.    The  nerve  supply  is  good,  but  the  gums  are 
not,  when  normal,  as  sensitive  to  pain  as  other  mucous  mem- 
branes, and  particularly  is  the  sensitiveness  reduced  in  the  pos- 

375 


376 


DENTAL   PATHOLOGY 


terior,  or  lingual,  portion  of  the  gum  due,  undoubtedly,  to  the  con- 
stant traumatism  it  is  subjected  to  in  the  process  of  mastication. 

GINGIVA 

Normal  and  Pathologic  Considerations 

By  the  term  gingivce  is  meant  that  extension  of  the  gum  tissue 
proper  which,  starting  at  the  crest  of  the  alveolar  process,  reaches 


Fig.  292. — Normal  gingiva  of  sheep.  The  relation  of  its  cellular  elements  is  similar 
to  that  in  the  human  structures.  The  cells  being  larger,  the  tissue  can  be  studied  more 
satisfactorily  than  in  the  human  specimen.  In  man,  the  horny  layer,  (stratum  corneum) 
is  not  nearly  as  prominent  as  it  appears  in  this  specimen,  a,  area  in  which  individual 
epithelial  cells  with  their  respective  nuclei  can  be  clearly  seen;  b,  stratum  germinativum 
or  stratum  Malpighii;  c,  connective  tissue  stroma;  d,  capillaries  in  connective-tissue 
papilla.      (Section  by  Dr.  A.   C.  La  Touche.) 

to  the  free  unattached  margin  of  the  gingiva?,  called  the  gingival 
border.  It  is  composed  of  (1)  the  body  of  the  gingivae,  or  that 
portion  which  is  attached,1  at  one  end,  to  the  crest  of  the  alveolar 
process  by  means  of  the  fibers  of  the  alveolar  periosteum,  and 


1G.   V.   Black's  classification. 


THE   GUMS    AND   GINGIWE 


377 


at  llic  oilier  to  thai  portion  of  the  root  between  the  alveolar 
crest  and  the  cementoenamel  junction  by  means  of  the  filters  of 
the  peridental  membrane;  of  (2)  the  \'n'v  gingivae,  or  thai  un- 
attached portion  of  tissue  which  extends  on  the  labial,  buccal  and 
Lingua]  surfaces  for  a  distance  of  from  one  to  live  millimeters; 
and  of  (3)    the  septal   gingivae,  or  that  portion  of  tissue  which 


Fig.  293. — Gingiv.-e  of  sheep.  The  arrangement  of  the  epithelial  and  connective  tis- 
sue structures  is  identical  to  that  found  in  man.  At  the  gingival  cul-de-sac  (subgingival 
fold)  in  man  the  epithelial  layer  becomes  thinner,  affording  little  protection  against  in- 
fectious agents  which  upon  breaking  through  the  epithelium  involve  the  underlying  con- 
nective tissue  mat  from  whence  the  possibility  of  metastasis  is  self-evident,  a,  stratum 
corneum,  or  horny  layer;  b.b,  stratum  germinativum  or  stratum  Malpighii;  c,  c,  capil- 
lary network  in  papilla  from  underlying  connective-tissue  stroma  (mat)  ;  d,  d,  connec- 
tive-tissue stroma;  c,  blood  vessel  in  stroma;  /,  epithelium  lining  internal  surface  of  gingi- 
val cul-de-sac,  g. 


almost  entirely  fills  up  the  interproximal  space  to  a  short  dis- 
tance from  the  contact  point,  and  which  springs  from  the  ap- 
proximal  portions  of  the  body  of  the  gingivae. 

To  the  gingiva?  are  attached  sets  of  fillers  from  the  peridental 
membrane  as  follows : 


378 


DENTAL   TATHOLOGY 


A  group  of  fibers  which  springs  from  the  peridental  membrane 
and  is  attached  to  the  body  of  the  gingivae;  a  group  of  fibers 
which  runs  a  little  below  the  alveolar  crest  and  connect  the  peri- 
dental membrane  of  one  tooth  with  that  of  another.  This  group 
of  fibers  passes  through  the  septal  gingivae.  A  group  of  fibers 
runs  from  the  peridental  membrane,  curving  at  first  in  an  oc- 
clusal direction  and  then  becomes  attached  to  the  crest  of  the  al- 
veolar process. 


Fig.  294. — Unman  gingiva.  The  dark  border,  a,  a,  is  the  stratified  squamous  epithelial 
lining.  Between  the  epithelial  prolongations  and  within  the  connective-tissue  papillae  are 
found  the  capillary  loops  at  b;  the  connective  tissue  stroma  at  c,  is  composed  of  connective 
tissue  fibers  and  of  round,  stellate,  and  spindle-shaped  cells.  The  epithelial  layer  being 
devoid  of  blood  vessels  its  nourishment  is  derived  by  osmosis  from  the  capillary  loops  in 
the  connective  tissue  papilla. 


Functions 

The  functions  of  the  gingivae  are  protective  so  far  as  the  peri- 
dental membrane  is  concerned.  They  encircle  the  tooth  in  its 
entirety  from  the  alveolar  crest  to  the  external  or  free  gingival 
border  over  a  distance  of  several  millimeters.  The  consistence 
and  contour  of  the  gingivae  favor  the  gliding  of  food  over  their 
surfaces  in  the  course  of  mastication,  with  the  minimum  of  lodg- 
ment of  debris  against  the  free  border,  and  this  protection  is 
further  augmented  by  the  crown  contour  commonly  described 


THE  GUMS  A\n  cixciv.i;  379 

as  bell-shaped.1  This  arrangement  exists  when  the  tissue 
is  qo1  subjected  to  abnormal  degrees  of  mechanical,  chemical,  or 
other  forms  of  irritation.  The  septal  tissues  depend  to  a  large 
extent  upon  the  character  of  the  contact  point  for  the  mainte- 
nance of  their  physiologic  function.  Lack  of  contact  or  broad 
contact,  between  two  approximal  surfaces  leads  in  time  to  dis- 
ease of  the  gingivae,  and  ultimately  to  involvement  of  the  periden- 
tal membrane  and  alveolar  process. 

Black  and  Xoyes  attach  considerable  importance  to  the  gin- 
givae in  maintaining  the  correct  relationship  of  the  teeth  to  each 
other  and  to  the  arches.  They  argue  that  following  the  extrac- 
tion of  a  tooth  a  mass  of  cicatricial  tissue  is  formed  at  the  point 
where  the  transseptal  fibers  are  attached,  (i.  e.,  the  peridental 
fibers  which  cross  from  the  peridental  membrane  of  one  tooth  to 
that  of  another),  and  that  the  contraction  of  this  tissue  moves  the 
adjacent  teeth  bodily  toward  one  another.  It  is  unquestionable 
that  disease  and  destruction  of  the  gingivae  bring  about  mal- 
position of  the  teeth,  as  frequently  seen  in  pyorrhea  alveolaris, 
where  a  tooth  will  move  in  a  direction  away  from  the  so-called 
pus  pocket.  This  is  due  to  the  fact  that  the  peridental  fibers  on 
the  affected  side  have  been  lost  or  destroyed,  the  pull  of  the 
group  of  fibers  on  the  opposite  tooth  surface  carries  the  tooth  away 
from  the  area  of  peridental  and  gingival  involvement.  Destruc- 
tion of  the  group  of  fibers  which  attaches  to  the  crest  of  the  alveolar 
process  results  in  the  extrusion  of  the  tooth,  a  phenomenon  observ- 
able in  pyorrhea  alveolaris. 

The  epithelium  which  covers  the  gingivae  exercises  under  nor- 
mal conditions,  a  protective  function  similar  to  that  which  per- 
tains to  the  epithelium  of  the  covering  of  the  body.  In  the 
ease  of  the  free  and  septal  gingiva?  the  epithelium  covers  its  ex- 
ternal surface  as  well  as  the  subgingival  space  (i.  e.,  that  sur- 
face in  contact  with  the  enamel  at  the  neck  of  the  tooth),  al- 
though upon  the  internal  aspect  the  stratum  corneum  (horny 
layer)  is  attenuated  or  absent.  In  people  who  are  careless  in  the 
hygiene  of  the  mouth,  food  debris  and  mucin  become  lodged 
against  the  free  border  of  the  gingiva?  and  there  undergo  de- 
composition, with  the  formation  of  acid  or  alkaline  end  products. 
The  gingivae  are  thus  at  first  merely  irritated ;  but  by  undergo- 


iFriesell,  H.  E- :     Jour.  National  Dental  Assn.,  vi,  579. 


380  DENTAL   PATHOLOGY 

ing-  a  decrease  in  their  power  of  resistance  by  reason  of  this  con- 
stant irritation,  they  soon  become  the  seat  of  bacterial  activity. 
Degeneration  and  death  of  the  epithelial  cells  lining  the  gingivae, 
particularly  of  those  lining  the  subgingival  space,  follow,  and 
these  tissues  and  the  underlying  connective-tissue  stroma  become 
not  only  the  seat  of  bacterial  activity,  but  also  an  active  source 
of  absorption  for  bacteria  and  their  toxins.  It  is  well  to  remem- 
ber that  the  papilla?  of  the  tunica  propria  contain  capillary  loops 
and  that  perivascular  lymph  spaces  are  also  present.  Absorption 
of  these  noxious  substances  occurs  by  the  hematogenic  or  lympho- 
genic routes,  or  by  both.  Clinically  the  writer  has  observed  and 
studied  a  large  number  of  patients  exhibiting  symptoms  of  gen- 
eral toxemia  and  of  infection  in  the  digestive  and  respiratory 
organs.  which  improved  markedly  by  proper  treatment  being 
directed  at  these  tissues;  viz..  the  subgingival  spaces.  While  the 
life  and  usefulness  of  the  peridental  membrane  depend  to  such  a 
large  extent  upon  the  health  and  integrity  of  the  gingival  tissues, 
again  the  latter  depend  for  their  own  health  and  physiologic  ef- 
ficiency upon  the  topography  of  the  teeth  and  the  character  of 
the  contact  between  the  approximal  surfaces.* 


*Hartzell  in  his  investigation  of  gingival  infections  and  subsequent  systemic  involve- 
ments has  thrown  considerable  light  on  the  absence  of  protectiveness  in  the  subgingival 
cul-de-sac.  The  reader  is  referred  to  his  writings  in  the  files  of  the  Journal  of  the 
National  Dental  Association. 


CHAPTEB  XXVI I 

CALCAKEOUS  DEPOSITS 

Calcareous  deposits  upon  the  surfaces  of  teeth  are  divided,  from 
the  standpoint  of  their  origin,  into  salivary  and  subgingival  (se- 
rnmal  and  sanguinary).  The  former  originate  entirely  from  the 
saliva,  the  latter  probably  partly  from  the  saliva  and  partly  from 
sources  other  than  the  saliva,  viz..  blood,  lymph,  and  pus.  Cal- 
careous deposits  throughout  the  body,  including,  of  course,  de- 
posits upon  the  crowns  and  roots  of  teeth,  are  invariably  composed 
of  an  organic  matrix  which  becomes  impregnated  with  inorganic 
suits.  The  organic  nucleus,  or  matrix,  is  the  binding  substance. 
In  the  month  the  organic  matrix  is  a  mixture  of  mucin,  epithelial 
a  Us,  food  debris,  and  bacteria.  In  the  ducts  of  the  salivary  glands 
the  calcareous  deposit,  when  present,  is  composed  of  an  organic 
matrix  made  up  of  a  thickened  secretion  of  the  epithelial  lining 
of  the  duct.1 

Calcareous  masses  in  the  intestines  are  formed  by  the  deposition 
of  calcium  phosphate,  calcium  carbonate  and  ammonio-magnesium 
phosphate,  in  varying  proportions:  arterioliths  (calcareous  depos- 
its in  the  arteries),  and  pkleboliths  (calcareous  masses  in  the 
veins),  are  due  to  the  calcification  of  thrombi.  It  will  therefore  he 
seen  that  the  general  arrangement  of  the  calculus  is  fundamentally 
identical,  no  matter  where  found. 

Two  theories  have  been  advanced  in  explanation  of  the  phenom- 
enon of  salivary  calculi  (tartar)  formation.  One  of  these  worked 
out  by  the  late  H.  H.  Burchard  is  based  upon  the  theory  that  the 
solubility  of  water  for  certain  salts  of  calcium  is  increased  when 
the  water  holds  carbon  dioxide  in  solution,  so  that,  upon  the  escape 
of  any  carbon  dioxide  from  solution,  any  amount  of  soluble  cal- 
cium salts  previously  held  in  solution  above  the  normal  amount 
which  the  water  can  hold,  will  be  precipitated.  He  argues  that 
the  saliva,  after  it  is  poured  into  the  month,  loses  its  carbon  dioxide 
contents,  and  that  calcium  salts,  particularly  calcium  phosphate, 
are  precipitated  upon  and  into  a  mass  of  organic  debris  compos.',! 


1Ziegler:     General   Pathology,    New   York.   Win.   Wood   &  Co. 

381 


382  DENTAL   PATHOLOGY 

of  mucin  shreds,  epithelial  cells,  food  debris  and  bacteria.  That 
the  end  product  of  carbohydrate  fermentation  constantly  going  on 
in  the  mouth,  especially  in  locations  in  which  food  debris  is  re- 
tained because  of  inaccessibility  to  the  toothbrush  or  to  muscle 
and  tongue  action,  furnishes  a  sufficient  amount  of  acid  to  pre- 
cipitate the  mucin;  and  that  this  precipitate,  together  with 
bacteria  and  desquamated  cells,  forms  the  organic  nucleus  which 
becomes  impregnated  with  calcareous  salts. 

Clinical  examinations  show  that  those  deposits  are  found  upon 
surfaces  in  proximity  to  the  openings  of  the  ducts  of  the  salivary 
glands,  namely,  the  buccal  surfaces  of  the  upper  molars  and  the 
lingual  surfaces  of  the  lower  central  and  lateral  incisors.  These 
deposits  occur  upon  surfaces  which  are  rough.  Congenital  or  ac- 
quired enamel  defects  are  to  be  constantly  borne  in  mind  in  con- 
nection with  the  slmly  of  the  prophylaxis  of  calcareous  deposits. 
A  tooth  surface  that  is  smooth  and  polished  does  not  favor  deposits  of 
tartar.  Also,  surfaces  which  are  constantly  subjected  to  friction 
in  the  course  of  mastication  by  the  tongue,  cheeks  or  lips  are,  as 
a  general  rule,  free  from  deposits.  Concerning  the  nature  of  tar- 
tar composition  Kirk2  analyzes  the  studies  of  Rainey,  Hartin?-. 
and  of  Ord,  explaining  that  when  certain  earthy  salts  are  pre- 
cipitated in  a  medium  containing  a  colloidal  substance  in  solu- 
tion the  resulting  precipitate,  instead  of  being  crystalline,  is  in 
the  form  of  minute  spheroidal  masses;  and  further,  that  as  the 
precipitation  progresses,  these  spheroidal  masses  increase  in 
diameter  so  that  adjoining  masses  grow  into  contact,  and  by 
accretion  of  new  material  these  spheroidal  masses  coalesce,  giv- 
ing rise  to  mulberry-like  bodies. 

Professor  Harting3  extended  his  experiments  and  showed  that 
when  the  precipitates  are  formed  in  egg  albumen,  blood  serum, 
or  a  solution  of  gelatin,  a  variety  of  forms  may  be  produced 
which  resemble  concretions  found  in  the  animal  body.  The 
basic  substance  or  matrix  which  results  after  deposition,  if  treated 
with  an  acid,  dissolves  out  the  inorganic  constituents  of  the  con- 
cretion, and  he  named  the  residue  calco-globulin.  The  spheroidal 
bodies  he  named  calco-globulin. 

As  has  already  been  shown,  the  mixed  saliva  contains  a  propor- 


-Kirk:      American   Textbook   of   Operative   Dentistry,    Philadelphia,    Lea   &   Febiger. 
3Ibid. 


CALCAKI'.OI   S    M.I'MSITS 


383 


tiou  of  calcium  salts  in  solution,  mos'1  of  which  is  calcium  phos- 
phate; and  consequently  the  main  inorganic  ingredienl  of  salivary 
deposits  is  calcium  phosphate.  Unmixed  parotid  saliva  deposits 
calcium  carbonate  on  standing.  Kirk  is  of  the  opinion  thai  as  a 
result  of  putrefactive  decomposition  in  the  mouth,  ammonia  is 
formed,  and  thai  the  ammonia  will  precipitate  calcium  phosphate 
Erom  its  acid  solution  as  calcium  ammonium  phosphate,  or,  when 
magnesium  phosphate  is  present  in  addition  to  calcium  phos- 
phate, also  as  ammonium  magnesium  phosphate,  a  salt  which 
is  found  to  lie  one  of  the  constituents  of  certain  forms  of  tartar. 
A  form  of  deposit  eaused  by  the  chewing  of  the  betel  nut  is 
of  rapid  formation  and  extremely  destructive  to  the  investing 
t  issues. 


Fig.  295. — Salivary  calculi  on  the  lingual  surfaces  of  the  roots  of  lower  cuspids.  The 
proximity  of  these  surfaces  to  the  mouths  of  the  ducts  of  the  submaxillary  and  sub- 
lingual glands  is  the  reason  for  their  vulnerability  to  these  deposits. 


In  essence,  the  theory  just  outlined  is  one  which  assumes  that 
the  organic  nucleus  of  the  salivary  deposits  is  furnished  by 
precipitated  mucin,  desquamated  epithelial  cells,  food  debris, 
bacteria,  etc.,  as  found  in  the  mouth;  and  that  the  inorganic  ma- 
terial is  furnished  by  the  saliva  which,  as  it  pours  into  the  mouth, 
loses  to  a  certain  extent  its  holding  power  for  a  number  of  inor- 
ganic salts,  particularly  tricalcium  phosphate  (Ca3  (P04)2).  G. 
V.  Black,  on  the  other  hand,  believed  that  calcareous  deposits 
upon  the  surfaces  of  teeth,  either  salivary  or  subgingival,  are 
formed  by  the  deposition  upon  slightly  roughened  surfaces  of 
teeth,  of  a  combination  of  an  organic  material  (possibly  a  globulin 


384 


DEXTAL    PATHOLOGY 


which  he  named  agglutinin  of  salivary  calculus)  with  inorganic 
salts.    In  this  theory  it  is  assumed  that  the  organic  and  inorganic 


Fig.  296. — Voluminous  salivary  calcu- 
lus with  shelf-like  formation  which  rested 
upon  the  mucous  membrane  of  the  floor 
of    the    mouth. 


Fig.    297. — Salivary    calculus    with    shelf 
iike    formation. 


Fig.  298. — Salivary  calculus  in  lower 
right  incisor  which  had  accumulated  to 
within  one-eighth  of  an  inch  of  the  apex. 
( (bserve  the  saddle-like  arrangement  of 
tin  deposit  Oil  the  lingual  aspect,  resting 
upon    the   soft    tissues. 


Fig.  299. — Salivary  calculus  which  had 
attained  considerable  size  and  had  caused 
the  exfoliation  of  the  tooth.  The  apical 
area    was    entirely    covered    by    the    deposit. 


elements  of  salivary  calculi  are  brought  together  into  the  mouth 
in  the  saliva  and  deposited  upon  the  surfaces  most  accessible  to 


c  UjCAREOUS  deposits 


:;>:. 


Fig.  300. — Salivary  cal- 
culus in  lower  incisor 
which  had  caused  the  ex- 
foliation   of   the    tooth. 


Fig.  301. — Salivary  cal- 
culus covering  all  of  the 
crown  and  most  of  the  root 
of  the  tooth. 


Fig.  302. — Salivary  cal- 
i  nl us  which  covered  a  large 
area  of  crown  surface  and 
all  of  one-half  the  root  sur- 
face, the  latter  upon  all  as- 
pects. 


Fig.  303. — Salivary  calculus 
on  lower  right  cuspid  involving 
approximately  two-thirds  of  the 
root. 


Fig. 

calculus 
I  lit      of 


304. — Salivary 
on  lingual  as- 
the     root     of    a 


lower    central    incisor. 


Fig.  305. — Salivary 

calculus  covering  a  por- 
tion of  the  labial  surface 
of  a  lower  right  central 
incisor  and  reaching  on 
the  disto-lingual  aspect 
over  one-half  the  length 
of  the  root.  The  invest- 
ing tissue  had  been  de- 
stroyed to  a  level  slightly 
beyond  the  lowest  edge 
uf   the   calculus. 


386 


DENTAL   PATHOLOGY 


the  ducts  of  the  salivary  glands.  He  found  that  the  deposit  will 
form  in  preference  upon  surfaces  of  teeth  which  have  lost  their 
natural  smoothness  or  polish,  and  also  that  while  the  quality  of 
the  ingested  food  played  a  small  part  in  the  production  of  calculi 
the  same  could  not  be  said  of  the  quantity. 

Salivary  deposits  vary  from  the  minutest  possible  particle  to 
such  a  size  as  to  cover  the  roots  of  several  teeth  from  the  gin- 
gival margins  to  the  apex  (Figs.  295-309).  They  do  not  occur 
in  every  mouth.  Some  individuals  are  practically  free  from  them, 
while  with  others  they  form  rapidly  in  spite  of  careful  brushing 
of  the  teeth.    They  vary  in  color  from  a  very  light  chalky  color 


Fig.  306. — Salivary  calculus  entirely 
covering  the  buccal  surface  of  the  crown 
and  one-half  the  length  of  the  roots  of  an 
upper   left   first   molar. 


Fig.  307. — Voluminous  salivary  .deposits 
upon  buccal  and  part  of  the  occlusal  sur- 
faces  of  an  upper  molar. 


to  a  deep  yellow.  The  yellowish  variety  is  usually  the  harder.  There 
is  a  gradual  increase  in  density  from  the  time  of  the  first  deposi- 
tion until  the  calculus  assumes  a  decidedly  hard  texture.  During 
the  beginning  of  their  formation,  varying  in  different  individuals 
from  a  few  days  to  a  few  weeks,  they  are  soft  and  may  be  re- 
moved by  a  thorough  brushing  of  the  teeth.  In  contact  with  the 
gingivae  as  they  invariably  are,  they  produce  degrees  of  irritation 
Avhich  lessen  the  power  of  the  tissues  to  ward  off  infection,  at 
the  same  time  rendering  the  field  a  favorable  one  for  bacterial 
activity. 


CALCAKKOl'S    DEPOSITS 


387 


Lesions  in  the  Investing  Tissues  Caused  by  Salivary  Calculi 

The  deposition  begins  a1  the  gingival  margin,  and,  following  a 

decrease  in  the  resistance  of  the  soft  tissues  by  virtue  of  the  me- 

chanical   irritation  induced  by  the  deposit,   bacteria  invade  the 

area.     An  inflammation  follows   which   results   eventually  in  a 


Fig.    308. — Large   masses   of   salivary    calculi   removed    from   the   teeth   to   which    they   were 

attached. 


Fig.  309. — Large  masses  of  salivary  calculi. 


destruction  of  those  peridental  fibers  which  are  attached  to  the 
gingiva,  with  a  loss  of  structure  in  the  alveolar  process  and  over- 
lying gum  tissues.  The  disappearance  of  the  alveolar  process, 
as  well  as  of  the  gingival  tissue,  is  the  result  of  an  absorption 
of  these  structures  consequent  upon  nutritional  interference,  but 
may  also  be  the  result  of  the  liquefaction  of  tissue  cells  incident 


388  DENTAL    PATHOLOGY 

to  bacterial  activity  in  the  part ;  or  it  may  be  the  result  of  both. 
The  deposit  is  at  first  located  upon  the  enamel  at  the  gingival 
margin,  but  as  destruction  of  the  peridental  fibers  occurs 
and  the  alveolar  process  and  the  gum  tissue  gradually  disappear, 
if  the  deposit  be  not  removed  it  will  increase  in  size  and  again 
impinge  upon  the  peridental  fibers,  so  that  the  now  receded 
alveolar  process  and  gingival  tissue  will  again  suffer  another 
series  of  pathologic  phenomena  similar  to  that  just  described. 
In  this  way  the  process  goes  on  unless  the  deposit  is  removed 
by  instrumental  means.  The  type  of  inflammation  which  these 
salivary  deposits  induce  in  the  investing  tissues  should  be  clearly 
differentiated  from  the  disturbances  induced  by  other  forms  of 
calcareous  deposits.  In  the  case  of  the  salivary  variety,  the 
destruction  of  the  investing  tissue  reaches  but  a  short  distance 
beyond  the  deposit,  and  when  the  teeth  are  thoroughly  scaled  and 
polished,  and  the  gum  tissue  properly  stimulated  by  suitable 
medication,  a  return  to  a  healthy  condition  is  invariably  the  case. 
The  gum  tissue  can  not.  however,  be  brought  back  to  its  original 
relation  with  the  gingival  margin.  The  denuding  of  the  ce- 
mentuni  will  be  permanently  established.  Attempts  have  been 
made  in  the  past  to  remedy  gum  recession  by  surgical  means,  but 
the  results  have  not  so  far  justified  the  means. 

P.  Rosenthal4  recommends  the  following  technic  to  remedy 
recession  of  the  gums — the  result  of  deposition  of  tartar,  trau- 
matism, erosion,  or  caries.  He  calls  attention  to  the  necessity  of 
first  restoring  the  surface  contour  of  the  tooth,  if  necessary,  by 
gold  fillings. 

"The  gum  above  the  tooth  to  be  operated  on  is  carefully  ster- 
ilized with  tincture  of  iodin.  and  a  horizontal  incision  is  made 
the  width  of  the  tooth,  at  right  angles  with  the  long  axis  and 
sufficiently  high  up  on  the  gum  to  furnish  a  good-sized  flap.  This 
incision  should  involve  the  periosteum.  The  flap  is  then  stripped 
off  the  bone  by  inserting  a  fine  instrument  under  it,  starting  at 
the  neck  of  the  tooth,  and  should  be  large  enough  to  allow  of  easy 
mobility.  A  silk  ligature  is  then  passed  under  the  central  por- 
tion of  the  flap  parallel  with  the  incision  and  taking  in  almost 
the  entire  breadth  of  the  flap.  Another  ligature  is  tied  tightly 
around  the  free  portion  of  the  tooth,  and  to  this  ligature  the  first 
ligature  is  secured,  the  flap  being  drawn  up  a  little  higher  than 

4Le   Laboratoire,    Paris,    November  26,    1911,   Dental   Cosmos. 


CALCAREOUS    DEPOSITS  389 

the  normal  gum  line  of  the  tooth  to  allow  For  a  recession  from 
cicatrization.  The  wound  and  the  ligature  are  painted  with 
tincture  of  iodin,  this  antiseptic  treatmenl  to  be  repeated  daily. 
Prom  the  second  day  on  the  gum  is  massaged  in  the  direction  of 
the  long  axis  and  toward  the  Five  portion  of  the  tooth.  On  the 
fifth  or  sixth  day  the  ligatures  are  removed.  As  a  rule,  cicatriza- 
tion is  then  sufficiently  advanced  to  prevent  recession  of  the  flap. 
The  primary  incision  would  fill  up  completely  without  leaving  a 
scar.  Rosenthal  claims  that  in  eases  kept  under  observation  for 
several  years  the  results  are  still  perfect. 

In  summarizing  the  effects  of  salivary  deposits  upon  the  in- 
vesting tissues,  it  must  be  stated  that  salivary  deposits  exercise 
a  detrimental  influence  by  reason  of 

1.  Mechanical  irritation  of  the  gingiva  and  peridental  mem- 
brane. 

2.  By  favoring  the  deposition  and  decomposition  of  food  par- 
ticles, either  fermentation  or  putrefaction,  or  both. 

3.  By  rendering  the  field  of  their  location  a  suitable  one  for 
bacterial  invasion — lowered  vital  resistance. 

The  products  of  these  processes  of  molecular  simplification — 
fermentation  or  putrefaction  of  food  particles — produce  a  degree 
of  irritation  in  the  investing  tissues  which  invites  bacterial  in- 
vasion.   Bacteria  play  a  leading  part  in  the  process. 

The  form  of  disturbance  caused  by  salivary  deposits — salivary 
calculi  gingivitis — may  be  localized  or  generalized  throughout  the 
mouth.  In  the  former  case  the  investing  tissues  over  one  or  a 
few  teeth  only  are  affected ;  in  the  latter  case  the  investing  tis- 
sues throughout  the  mouth  are  affected.  The  clinical  symptoms 
of  salivary  calculi  gingivitis  are: 

1.  Disappearance  of  the  gingiva  and  gums  as  the  result  of 
pathologic  absorption  (atrophy),  bacterial  activity,  or  both. 

2.  Congestion  and  tumefaction  of  the  gingiva  and  gums. 

3.  Bleeding  at  the  slightest  provocation. 

4.  A  change  in  the  color  of  the  tissues  from  a  healthy  pink  to 
a  deep  red,  purple,  or  bluish  black. 

5.  Putrefactive  and  fermentative  changes. 

6.  Tenderness  or  pain  upon  mastication,  or  upon  the  intro- 
duction of  irritating  articles  of  food. 

7.  Fetor  of  breath. 

8.  Svstemic  involvement. 


CHAPTER  XXVIII 

SUBGINGIVAL  DEPOSITS 

Etiology 

Subgingival  deposits  are  those  which  are  in  the  first  place 
formed  under  the  free  gingiva.  They  are  of  a  darker  color  than 
the  salivary  deposits  and  are  also  harder.  The  darker  the  de- 
posit, the  more  adherent  it  is  to  the  root.     They  are  evidently 


Fig.  310. — An  upper  lat-  Fig.       311. — Subgingival  Fig.       312. — Subgingival 
eral    incisor    with    its    root  deposits  in  upper  right  lat-         deposits  in  upper  right  dis- 
covered    with      subgingival  eral    incisor,    distal    view.              pid. 
deposits    over    half    of    its 
length. 

the  result  of  an  abnormal  degree  of  irritation  of  the  gingival 
tissues  (Figs.  310-316).  The  irritation  is  afforded  by  the  de- 
composition of  food  debris  and  mucin  at  the  necks  of  the  teeth, 
by  ragged  or  rough  edges  of  fillings,  poorly  adapted  gold  crowns, 
or  from  any  other  form  of  prosthetic  appliance  or  defective  res- 
toration leaving  a  rough  edge  at  the  neck  of  the  tooth  which 
continually  irritates  the  gingiva.  Any  form  of  injury  to  the  gin- 
giva may  become  the  etiologic  factor  in  the  deposition  of  subgin- 

390 


SUBGINGIVAL   DEPOSITS  391 

gival  deposits.  Gingival  irritation  is  not,  however,  by  any  means 
entirely  due  to  defective  crowns  or  fillings,  but  may  be  broughl 
about  by  defective  or  insufficient  contact  points  leading  to  food 
impactions  in  the  interproximal  spaces,  with  concomitant  irri- 


Fig     313.— Subgingival    deposits    in  Fig.    314.— Subgingival    deposits    in 

unper  right   second   molar.  uPP.er    rlSht    second    molar       These    de- 

posits were  greenish  in  color  and  sur- 
rounded the  tooth  at  the  enamel-ce- 
mentum  junction  upon  all  of  its  sur- 
faces   except    the    lingual. 


Fig.    315. — Roots    of    a    molar    cov-  Fig.    316. — Subgingival    deposits    on 

ered   with    subgingival    deposits.  the    anterior    and    posterior    roots    of    a 

lower   molar. 

tation  of  the  gingiva? ;  they  likewise  may  be  induced  by  the  pres- 
ence of  salivary  calculi.  Salivary  and  subgingival  deposits  may 
be  found  upon  the  same  tooth,  the  supposition  being  that  the 


392  DENTAL   PATHOLOGY 

salivary  deposit  was  formed  first  and  the  other  occurred  fol- 
lowing the  gingival  irritation  induced  by  the  former.  It  is  not 
infrequent  that  patients  have  their  teeth  sealed  and  polished 
and  consequently  have  the  salivary  deposits  entirely  removed, 
while  the  subgingival  deposits  remain  untouched.  In  this  way 
Ave  may  in  part  account  for  the  fact  that  in  a  number  of  in- 
stances the  subgingival  deposit  is  found  while  the  salivary  is  not 
to  be  seen. 

The  subgingival  deposit,  once  formed,  irritates  the  gingiva, 
thereby  inviting  bacterial  activity.  As  the  result  of  the  infection, 
the  peridental  fibers  are  destroyed  so  that  additional  deposils 
of  calculi  will  form  and  encroach  upon  the  still  attached  border 
of  the  peridental  membrane.  Infection  will  become  active  again 
and  more  peridental  fibers  will  be  destroyed,  the  process  ad- 
vancing in  this  way  until  a  so-called  "pocket"  results.  This  proc- 
ess of  pocket  formation  is  decidedly  chronic  in  the  sense  that 
it  is  of  slow  formation,  years  elapsing  in  most  cases  before  a 
well-formed  pocket  is  present.  It  is  not  to  be  assumed,  how- 
ever, that  in  the  presence  of  any  one  or  several  of  these  etiologic 
factors,  subgingival  deposits  will  be  invariably  present.  The 
inorganic  salts  in  suitable  amount  must  be  present  in  the  gin- 
gival exudate  and  the  conditions  leading  to  the  formation  of  the 
organic  matrix  must  be  present,  and  then  this  takes  place  only 
when  the  body  metabolism  is  disturbed,  even  though  only  slightly. 

LESIONS  PRODUCED  BY  SUBGINGIVAL  DEPOSITS: 
CHRONIC  GINGIVITIS 

Pathologic  Anatomy 

The  student  should  bear  in  mind  the  striking  difference  in  the 
character  of  the  effect  upon  the  investing  tissues  of  salivary  de- 
posits and  of  subgingival  deposits  as  originally  pointed  out  by 
G.  V.  Black.  In  the  former,  well-defined  pus  pockets  are  rare, 
while  in  the  latter  form  pockets  almost  invariably  follow.  The 
early  deposition  of  subgingival  calculi  can  be  detected  by  the 
color  of  the  gingivae,  which  are  of  a  deep  red,  in  some  instances 
running  to  a  blue,  purple,  or  even  black.  The  tissues  are  flabby 
and  present  an  appearance  typical  of  a  chronic  inflammation. 
The  stratified  squamous  epithelium  dips  into  the  connective  tis- 


SI   BGINGIVAL    DEPOSH  - 


:;:»:; 


sue  to  a  greater  Length  than  is  the  case  with  normal  epithelium, 
and  the  connective-tissue  mat  of  the  mucous  membrane  is  almost 
everywhere  infiltrated  with  Large  masses  of  round  cells,  most  of 
which  are  mononuclear  Leucocytes,  large  and  small,  plasma  cells, 
lymphocytes  and  polymorphonuclear  leucocytes  in  small  numbers 
(Figs.  317,  318  and  319).  Mast  cells  so  often  found  in 
mucous  membranes  which  are  the  seat  of  chronic  inflammation 


Fig.  317.— Section  of  human  gingiva.  The  stratified  squamous  epithelium  has  lost 
its  characteristic  appearance;  the  projections  of  epithelial  cells  between  the  papillae  of 
connective  tissue  have  become  elongated.  The  gingiva  was  the  seat  of  a  chronic  inflam- 
mation which  by  continuity  involves  the  peridental  membrane  and  the  alveolar  process. 
It  marks  the  beginning  of  pocket  formation.  a,  a,  elongated  epithelial  projections;  b, 
connective-tissue  stroma. 


are  also  to  be  seen.  The  infection  spreads  slowly  as  a  general 
rule,  and.  involving  the  fibers  of  the  peridental  membrane  and  the 
alveolar  process,  initiates  the  progressive  process  of  destruction 
in  the  supporting  tissues  of  the  tooth  (Figs.  320-325).     The  pus 


594 


DENTAL   PATHOLOGY 


pocket  is  the  result  of  the  destruction  of  the  peridental  fibers 
and  of  the  alveolar  process.  The  proteolytic  toxins  formed  in 
the  course  of  the  inflammatory  process  liquefy  the  peridental 
fibers. 

The  pathologic  phenomena  which  develop  in  the  bone  of  the 
alveolar    process    in    pocket    formation    are    characteristic    of    an 


// 


Fig.  318. — Chronic  inflammation  of  gingiva.  The  epithelial  prolongations  in  the  sub- 
jacent connective  tissue  elongate  as  the  result  of  the  continued  low  degree  of  irritation. 
The  connective-tissue  stroma  has  lost  its  characteristic  appearance  and  the  cells  and  fibers 
which  were  present  under  normal  conditions  have  been  replaced  by  inflammatory  cells; 
i.  e.,  mononuclear  wandering  cells  comprising  mononuclear  leucocytes,  lymphocytes,  and 
plasma  cells  and  polymorphonuclear  leucocytes  in  small  numbers,  a,  a,  elongated  epithelial 
projections;  b,  b,  round  cell  infiltration.  Mast  cells  are  also  to  be  located  under  the 
higher   magnifications. 


infectious  osteomyelitis.  The  medullary  substance  contained  in 
the  cancellated  spaces  becomes  the  seat  of  a  chronic  inflamma- 
tion in  which  osteoclasts  play  an  active  part.  The  hard  sub- 
stance  of  the  bone  disappears  through  osteoclastic  action,  the 


SUBGINGIVAL    DEPOSITS 


395 


cancellated  spaces  are  eaten  through,  and  the  Haversian  canals 
widened.  The  contents  of  the  spaces  become  filled  with  large 
masses  of  inflammatory  cells,  viz.,  mononuclear  and  polymorpho- 
nuclear leucocytes,  lymphocytes,  plasma  cells,  and  giant  cells.  Suc- 
cessively the  bone  lamellae  are  destroyed  or  carried  away  by  osteo- 
clasis and  the  inflamed  medullary  contents  of  the  canal  breaks  down. 


Fig.  319. — Chronic  inflammation  of  the  free  gingiva.  The  tissue  has  lost  all  its 
histologic  characteristics  and  is  gradually  disappearing  as  the  result  of  interference  with  its 
nutrition,   and   cell   liquefaction. 

Kirk1  believes  that  "the  principles  governing-  the  precipitation 
of  earthy  phosphates  and  carbonates  directly  from  the  saliva 
in  the  production  of  true  salivary  tartar  govern  also  the  pro- 
duction of  the  girdle-like  concretions  that  are  found  encircling 
the  teeth  at  and  below  the  anatomic  neck  and  beneath  the  gum 


IKirk:     American  Text-book  of   Operative  Dentistry,   Philadelphia,   Lea  &   Febiger. 


396 


DENTAL   PATHOLOGY 


margin."  The  preliminary  step  in  the  formation  of  subgingival 
deposit  this  investigator  attributes  to  the  retention  under  the 
gingival  tissues  of  an  inflammatory  exudate  rich  in  colloid  ma- 
terial, the  latter  being  the  binding  material  of  the  deposit,  giv- 
ing to  it  its  characteristic  hardness.     The  difference  in  color  be- 


Fig.  320. — Gingivitis,  chronic,  advanced  stage,  the  infection  is  progressing  toward  the 
peridental  membrane,  a.  dentin;  b,  cementum;  c,  c,  stratified  squamous  epithelium  lining 
subgingival  space;  d,  d,  fillers  of  peridental  membrane  in  the  gingiva;  e,  e,  round  cell  in- 
filtration. 


tween  salivary  and  subgingival  deposits  is  believed  to  be  due 
to  the  formation  of  sulphomethemoglobin;  the  source  of  the 
hemoglobin  is  from  the  disintegration  of  erythrocytes,  and  the 
sulphur  from  the  putrefactive  changes  in  nitrogenous  food  re- 
tained at  the  gingival  margin. 


KUP.UINUIVAL    DKI'OSITS 


397 


Tu  sections  of  the  gingivae  the  Layer  of  stratified  squamous  epi- 
thelium and  1  lie  epithelial  prolongations  into  1  he  underlying  connec- 
tive tissue  assume  unusual  Conns  by  reason  of  a  pronounced  pro- 
liferation of  epithelial  cells  and  also  on  account  of  the  level  at 
which  the  section  is  cut.  In  the  interpretation  of  sections  of  a 
gingiva  which  has  been  the  seat  of  a  chronic  infectious  process,  these 
facts  should  be  borne  in  mind. 


Fig.  321. — Gingivitis,  chronic,  advanced  stage,  induced  by  subgingival  deposits,  a, 
subgingival  cul-de-sac;  b,  b,  portions  of  stratified  squamous  epithelium  from  the  internal 
lining  of  the  gingival  cul-de-sac;  c,  break  in  the  epithelial  layer  marking  one  of  the 
portals  of  the  infection  (the  bit  of  tissue  projecting  out  was  torn  in  mounting  the  section)  ; 
d,  d,  round-cell   infiltration;  e,  fibers  in  the  connective-tissue  stroma. 


rjOS 


DENTAL   PATHOLOGY 


f- 


k  * 


**        ■*.. 


\ 


Fig.  322. — Progressive  chronic  gingivitis.  Decalcified  longitudinal  section.  The  in- 
fection which  originated  at  the  gingival  margin  has  advanced  to  where  the  peridental 
membrane  begins.  It  is  only  a  matter  of  time  before  the  peridental  fibers  which  are 
attached  to  the  crest  of  the  alveolar  process  will  become  involved,  a,  alveolar  septum; 
b,  crest  of  alveolar  process;  c,  peridental  fibers  which  are  attached  to  the  crest  of  the 
alveolar -process;  d,  dentin;  e  and  /,  areas  of  round-cell  infiltration  marking  the  progress 
of  the  infection. 


SUBGINGIVAL    DEPOSITS 


399 


Fig.  323. — Chronic  inflammation  of  gingiva.  The  light  area  at  the  lower  section  of  the 
picture  is  the  subgingival  cul-de-sac.  To  the  left  of  the  picture  a  portion  of  cementum 
and  dentin  is  to  be  seen,  while  to  the  right  of  the  picture  is  the  gingiva  and  gum.  a, 
subgingival  space;  b,  dentin;  c,  cementum;  d,  epithelium  of  subgingival  space;  e,  point 
at  which  infection  has  brought  about  liquefaction  of  epithelial  lining;  f,f,f,  areas  of 
round-cell  infiltration.      (Chronic  inflammation.) 


400 


DENTAL    PATHOLOGY 

b 


/•-...- 


Fig.  324. — Chronic  inflammation  in  the  gingiva  which  has  spread  to  the  peridental 
membrane.  An  area  of  marked  chronic  involvement  (round-cell  infiltration  i  is  seen 
in  the  horizontal  peridental  fibers,  a,  a,  alveolar  process;  b,  b,  cementum;  d,  d,  horizon- 
tal fibers  of  the  peridental  membrane;  e,  an  area  of  involvement  which  includes  some  of 
the  horizontal   fibers  of  the  peridental  membrane. 


Sl'l!(il\(il\   \l,    DKI'OSITS 


401 


Fig.  325. — Progressive  chronic  gingivitis,  a,  cementum;  b,  space  produced  by  detach- 
ment of  cementum  from  dentin  in  process  of  decalcification  and  sectioning;  d,  fibers 
running  from  peridental  membrane  into  gingiva;  c,  f,  and  g,  stratified  squamous  epithe- 
lium lining  internal  surface  of  gingival  cul-de-sac;  h  and  i,  round-cell  infiltration  in 
gingiva  (chronic  inflammation)  progressing  in  the  direction  of  the  fibers  of  the  peri- 
dental membrane  at  /  and  d. 


CHAPTER  XXIX 

DISEASES  OF   THE   PERIDENTAL  MEMBRANE 

The  peridental  membrane,1  or  pericementum  (alveole-dental  peri- 
osteum, or  root  membrane)  is  a  fibrous  structure  with  a  rich  vas- 
cular and  nerve  supply,  devoid  of  elastic  fibers,  encircling-  the 
root  of  the  tooth  in  its  entirety,  and  attached  to  the  cementnm 
by  means  of  fibers  which  bear  the  same  relation  to  the  cementnm 
as  the  periosteal  fibers  of  Sharpey  do  to  bone  (Figs.  326,  327  and 
328). 

The  functions  of  the  peridental  membrane  are: 

1.  To  act  as  the  means  of  attachment  of  the  tooth  to  the  al- 
veolus. 

2.  To  exercise  a  cushion-like  function,  thereby  protecting  the 
more  sensitive  internal  organ  of  the  tooth,  i.e.,  the  pulp,  from 
traumatism  such  as  would  result  from  mastication,  blows,  etc. 

3.  To  act  as  a  nourishing  periosteum  to  the  cementnm  and  as 
the  source  of  collateral  circulation  to  the  alveolus. 

4.  To  maintain  the  gingival  contour  by  virtue  of  the  arrange- 
ment of  its  fibers  at  the  neck  of  the  tooth. 

5.  To  absorb  and  build  alveolar  bone  and  cementum  during  the 
life  of  the  tooth  in  response  to  degrees  of  stimulation,  and  until 
such  time  as  occlusion  has  been  permanently  established. 

6.  Tactile  function. 

It  is  thicker  near  the  neck  of  the  tooth  and  in  the  apical  re- 
gion, but  becomes  thinner  throughout  with  age.  This  fact  ac- 
counts for  the  greater  susceptibility  of  the  peridental  membrane 
to  infectious  processes  in  the  middle-aged  and  the  old.  With  a 
thinning  of  the  membrane  there  occurs  a  decrease  in  the  num- 
ber and  in  the  caliber  of  arteries  and  capillaries,  and  the  less- 
ened circulation  in  the  membrane  renders  more  difficult  or  im- 
possible the   warding   off  of  infectious  processes. 

The  blood  supply  of  the  pulp  and  that  of  the  peridental  mem- 
brane are  intimately  associated.    This  consists  of  a  variable  num- 


nVe    are   indebted    to    the   late   Dr.    G.    V.    Black   ami    to   Dr.    F.    B.    Noyes    for    their 
valuable  investigations  of  the  histologic  elements  of  the  peridental  membrane. 

402 


MSKASKS    OF    Till:    PERIDENTAL    MEMBRANE 


4<>:J 


ber  of  arteries  and  veins  (as  a  rule  one  main  artery  and  its 
vein,  but  occasionally  more  than  one),  passing  through  the  apical 
foramen  into  the  pulp  where  it  undergoes  ramifications;  the  other 
two  or  more  arteries  and  their  respective  veins  are  distributed 
to  the  peridental  membrane.  They  follow  in  the  peridental  mem- 
brane a  direction  parallel  to  the  long  axis  of  the  tooth,  break- 
ing up  into   arterioles   and   capillaries   which   encircle   the   mem- 


Fig.  326. — Normal  peridental  membrane,  prepared  by  carefully  detaching  the  peri- 
dental membrane  from  a  freshly  extracted  tooth  in  which  no  pathologic  processes  had 
taken  place.  Notwithstanding  the  care  in  dissecting  the  peridental  membrane  some  layers 
of  cementum  were  removed  unsuspectingly  and  are  shown  in  the  section.  That  scaling 
of  root  surfaces  without  removing  some  of  the  cementum  is  an  impossibility  is  confirmed 
by  this  section,  a,  a,  cementum  lamelhe;   b,  b,  normal  fibers  of  the  peridental  membrane. 


brane  in  its  entirety.  The  peridental  membrane  is  brought  into 
close  relationship  with  the  gingiva  from  the  crest  of  the  alveolar 
process  to  the  cementoenamel  junction,  by  means  of  the  alveolar 
crest  fibers.  These  fibers  run  from  the  peridental  membrane  into 
the  body  of  the  gingiva  and  are  attached  to  the  fibers  of  the  al- 
veolar periosteum  as  they  turn  over  the  crest  of  the  alveolar 
process.  In  addition,  the  peridental  membrane  sends  into  the 
gingiva  the  free  gingiva  groups  of  fibers,  and  across  the  septal 


404 


DENTAL    PATHOLOGY 


gingiva   the   transseptal   fibers   which   run   from   the   peridental 
membrane  of  one  tooth  to  that  of  the  next. 

The  fibers  of  the  peridental  membrane  are  wavy  or  un- 
dulated in  order  to  enable  the  tooth  to  have  a  certain  amount 
of  play  in  its  alveolus  without  traumatizatiou  of  the  fibers.  They 
may  for  convenience  of  description  be  divided  into  the  intraal- 


c 
d 
e 

d  ___. 

C 

fi 

Fig.  327. — Normal  peridental  membrane  in  situ,  a,  dentin;  b,  b,  cementum;  c,c,  peri- 
dental membrane;  d,  d,  d,  cancellated  spaces  in  alveolar  process;  c,  c,  c,  compact  or 
Haversian  bone. 


veolar  and  the  extraalveolar  fibers.  The  intraalveolar  fibers  pass 
into  the  substance  of  the  cementum  and  of  the  alveolus  for  pur- 
poses of  firm  attachment,  and  are  the  prototypes  of  Sharpey's 
fibers  in  periosteum.  They  comprise  the  horizontal  fibers,  the 
oblique  fibers,  and  the  apical  fibers. 


DISEASES    OF    TIIK    PERIDENTAL    MFIVIBRANE 


405 


Horizontal  Fibers.  -Horizontal  fibers  are  a  narrow  group  of 
fibers  attached  to  the  eementum  at  one  end  and  to  the  alveolar 
process  al  the  other,  occupying  a  space  immediately  beyond  the 
alveolar  crest.  Their  function  is  to  support  the  tooth  againsl 
lateral  displacements,  and  to  assist  in  preventing  rotary  move- 
ments of  the  tooth. 


Fig.  328. — Normal  peridental  membrane  and  its  relation  to  eementum  and  alveolar 
process,  a,  a,  peridental  membrane;  b,  b,  eementum;  d,  d,  lamellae  of  alveolar  process 
(compact  or   Haversian  bone). 

Oblique  Fibers. — Oblique  fibers  run  obliquely  from  the  ee- 
mentum to  the  alveolar  bone  and  constitute  the  bulk  of  the  mem- 
brane. The  attachment  of  the  fibers  at  the  eementum  is  at  a 
higher  level  than  in  the  alveolar  process  in  the  case  of  the  upper 
teeth  and  at  a  lower  level  in  the  case  of  the  lower  teeth.  Their 
function  is  to  support  the  tooth  against  occlusal  impactions.  Some 
of  these  fibers  run  direct  to  the  alveolar  process  without  split- 


406  DENTAL   PATHOLOGY 

ting  into  smaller  fibrillse;  others  split  into  fibrillae  which  are 
joined  together  for  attachment  at  the  alveolar  process. 

Apical  Fibers. — Apical  fibers  are  a  continuation  of  the  oblique 
fibers  which,  by  altering  their  course  for  a  more  direct  approach 
to  the  alveolar  process,  assume  a  fan-like  distribution.  Around 
the  apical  area  of  the  tooth  these  fibers,  together  with  the  con- 
nective-tissue cells  between  them  and  blood  vessels  and  nerves, 
constitute  the  periapical  tissues. 

The  extraalveolar  fibers  comprise  the  alveolar  crest  fibers,  the 
free  gingiva  fibers  (unattached  at  the  gingival  extremities),  and 
the  transseptal  fibers. 

Alveolar  Crest. — Alveolar  crest  fibers  follow  for  a  short  distance 
in  a  direction  at  right  angles  to  the  long  axis  of  the  tooth  curv- 
ing in  an  apical  direction  for  attachment  at  the  crest  of  the 
alveolar  process. 

Free  Gingiva. — Free  gingiva  fibers  are  unattached  at  their 
terminations  in  the  free  gingiva  and  septal  tissues.  The  group 
which  penetrates  the  septal  tissues  is  known  as  the  septal  fibers. 

Transseptal  Fibers. — Transseptal  fibers  take  a  course  immedi- 
ately under  the  alveolar  crest  fibers  on  the  approximal  aspects  of 
the  tooth,  and  are  attached  to  the  peridental  membrane  of  the  ad- 
jacent tooth. 

This  classification  of  the  fibers  of  the  peridental  membrane  into 
groups  is  not  to  be  discerned  in  every  specimen  studied  microscopi- 
cally. It  should  indeed  be  accepted  pretty  much  as  a  theory  which 
satisfactorily  explains  the  forces  which  tend  to  maintain  the  tooth  in 
its  alveolus  and  enable  it  to  have  a  limited  movement  in  certain  di- 
rections. In  the  average  sectioned  specimen  of  peridental  mem- 
brane in  situ  this  arrangement  of  its  fibers  can  not  be  discerned 
at  all,  or  only  with  considerable  difficulty.  That  some  such  ar- 
rangement as  above  described  actually  occurs  and  is  micro- 
scopically visible,  there  is  no  doubt;  but  the  variations  therefrom 
in  arrangement  and  disposition  are  also  numerous. 

The  Structural  Constituents  of  the  peridental  membrane  are: 

1.  White  fibers,  i.e.,  apical,  oblique,  horizontal,  alveolar  crest, 
transseptal  and  free  gingivae,  the  latter  including  the  septal 
fibers. 

2.  Fibroblasts,  i.e.,  spindle-shaped  connective-tissue  cells  occu- 
pying positions  parallel  to  the  long  axis  of  the  tooth  or  almost 
any  other  direction. 


DISEASES   OF   THE    PERIDENTAL    MEMBRANE  407 

3.  Cementoblasts — cementum-building  cells  located  on  the  ce- 
mentum  side  of  the  membrane. 

4.  Osteoblasts — alveolar  tissue  building  cells — located  on  the 
alveolar  side  of  the  peridental  membrane. 

5.  Osteoclasts — alveolar  tissue  resorbing  cells,  large  multi- 
nucleated cells  lying  at  points  along  the  alveolar  side  of  the 
peridental  membrane. 

6.  Cementoclasts — cementum  resorbing  cells  presenting  the 
same  characteristics  as  the  osteoclasts,  but  located  on  the  cemen- 
tum side  of  the  membrane  and  concerned  in  the  process  of  ce- 
mentum resorption. 

7.  Epithelial  debris — remnants  of  the  enamel  organ. 

8.  Blood  vessels  and  nerves.  An  arterial  trunk  branches  out 
into  a  number  of  arteries  before  it  penetrates  the  tooth.  One  or 
more  of  these  enters  the  root  canal  and  the  others  run  up  on 
each  side  of  the  peridental  membrane  and  branch  out  into  a 
veritable  network  of  capillaries  which  at  the  crest  anastomose 
with  the  blood  vessels  of  the  gingiva  and  gums.  The  nerves  fol- 
low an  analogous  course.  Blood  vessels  also  enter  the  peridental 
membrane  from  the  alveolar  process  and  pass  out  from  the  peri- 
dental membrane  into  the  alveolar  process,  thus  affording  to  the 
peridental  membrane  a  collateral  circulation  from  the  alveolar 
bone,  rendering  it  possible  for  the  peridental  membrane  to  live 
after  the  apical  circulation  and  the  anastomoses  with  the  blood 
of  the  gingiva)  and  gums  have  been  destroyed  by  infective  proc- 
esses or  by  surgical  intervention. 

The  fibroblasts  are  the  cells  which  form  the  white  fibers  of 
the  peridental  membrane.  These  cells  are  spindle-shaped  and 
their  number  decreases  with  age.  The  cells  occupy  places  be- 
tween the  fibers. 

The  cementoblasts  are  the  cementum-building  cells  and  are  to 
be  found  between  the  white  fibers  of  the  peridental  membrane. 
They  are  irregular  in  outline. 

The  osteoblasts  are  the  bone-building  cells,  and  those  which  are 
to  be  found  in  the  peridental  membrane  represent  the  remains  of 
a  group  of  cells  that  were  concerned  in  the  building  up  of  the 
alveolar  structure. 


CHAPTER  XXX 

NONSEPTIC  PERICEMENTITIS 

By  nonseptic  pericemental  inflammation  is  to  be  understood 
that  the  peridental  membrane  or  pericementum  has  become  the 
seat  of  vascular  changes  following  abnormal  degrees  of  irrita- 
tion from  which  bacterial  influences  are  excluded.  It  may  begin 
at  the  gingival  margin  and  spread  to  the  entire  membrane,  or 
at  the  apex  and  likewise  involve  the  organ  throughout  its  entire 
extent. 

The  causes  of  nonseptic  pericemental  inflammation  may  be 
enumerated  as  follows: 

Root  fillings  protruding  through  the  apical  foramen,  broaches, 
etc.;  the  introduction  of  medicaments  into  the  root  canal  which 
upon  evaporation  bring  about  a  degree  of  irritation  from  which 
the  pericemental  fibers  are  unable  to  quickly  recover;  the  mal- 
lethig  of  gold  fillings;  the  artificial  separation  of  teeth  for  op- 
erative purposes;  the  use  of  clasps,  etc.;  the  construction  of 
fillings  which  interfere  with  the  normal  articulation  of  the  tooth 
with  its  opponent;  the  impingement  upon  the  gum  and  peridental 
membrane  by  crowns,  clasps,  clamps,  and  other  appliances;  rapid 
movement  of  teeth  for  orthodontic  purposes. 

The  use  of  any  irritating  drug  which  under  ordinary  circum- 
stances will  cause  marked  irritation  of  soft  tissues  in  other  parts 
of  the  body,  should  be  avoided  in  root  canal  medication,  or  so 
modified  in  its  degree  of  concentration  as  to  produce  the  least 
degree  of  tissue  injury  compatible  with  germicidal  efficiency. 
For  instance,  the  irritating  effect  of  an  otherwise  so  efficient  a 
germicide  as  formaldehyde,  or  such  of  its  preparations  as  trioxy- 
methylene,  is  pronounced;  formaldehyde  in  any  form  disorgan- 
izes protein  matter  readily,  and  therefore  its  employment  in 
solutions  of  strong  concentration  defeats  the  purpose  for  which 
formaldehyde  is  generally  employed  in  root  canal  therapeutics. 
Verily  it  destroys  microorganic  life,  but  it  does  this  simultane- 
ously with  a  partial  or  complete  disorganization,  not  only  of  the 
periapical  tissues,  but  also  of  the  surrounding  alveolar  structures. 

408 


NONSEPTIC    PERICEMENTITIS  409 

From  the  standpoint  of  practical  efficiency,  it  is  not  alone  neces- 
sary that   a  chemical  substance  should   invariably  kill  bacteria, 

but  it  is  likewise  of  importance  that  it  should  do  Ibis  with  the 
least  possible  impairment  of  the  functions  of  the  healthy  cells 
with  which  the  antiseptic  must  come  in  contact.  We  surmise 
that  the  tendency  to  overlook  this  point  is  just  the  echo  of  the 
practitioner's  bacteriologic  conception  of  inflammatory  disorders, 
to  the  exclusion  of  the  factors  that  render  possible  bacterial  in- 
vasion with  its  attendant  reactions. 

In  the  seat  of  an  inflammatory  process,  whether  acute  or 
chronic,  it  is  of  the  utmost  importance  that  the  cellular  elements 
be  maintained  at  their  maximum  degree  of  functional  activity 
in  order  that  the  defensiveness  of  the  area  and  the  opportunities 
for  recovery  be  at  their  highest.  If  the  functional  efficiency  of 
the  cells  of  the  periapical  tissues  is  lessened  by  virtue  of  hav- 
ing been  exposed  for  some  time  to  substances  which  coagulate 
their  protein  contents,  or  which  deoxidize  or  dehydrate  their 
protoplasm,  or  in  some  other  way  alter  their  physical  or  chemical 
characteristics,  the  outcome  is  bound  to  be  detrimental  to  the 
future  efficiency  of  the  tooth.  The  effect  of  strong  germicidal 
concentrations  upon  the  delicate  periapical  tissues,  made  up  of 
the  fan-like  arrangement  of  the  peridental  fibers  which  begin  at 
a  point  where  the  surfaces  of  the  root  begin  to  converge  to- 
ward the  apex,  plus  blood  and  nerve  supply,  and  interfibrillar 
connective-tissue  cells,  is  manifested  in  a  series  of  degenerative 
changes  eventually  ending  in  their  death.  Furthermore,  the 
partial  or  complete  interference  with  the  chemical  mutations 
in  protoplasm  results  in  the  presence,  in  the  osseous  tissue  im- 
mediately surrounding  the  periapical  tissues,  of  areas  of  partly 
or  completely  devitalized  bony  structure  which  act  as  a  source 
of  continuous  irritation  to  the  as  yet  healthy  adjacent  tissue, 
so  that  eventually  the  resistance  to  bacterial  invasion  becomes 
subnormal.  There  is  little  doubt  that  areas  which  have  been 
subjected  to  the  action  of  strong  germicides  become  at  some 
future  time,  bacteria  being  available,  foci  of  chronic  in- 
fection. As  all  steps  in  root  canal  operations  are,  in  only 
a  small  number  of  instances,  performed  with  due  regard  to  strict 
asepsis ;  and  furthermore,  as  foci  of  infection  may  develop  in  the 
jaws  as  the  result  of  bacterial  invasion  via  the  circulation  and 


410  DENTAL   PATHOLOGY 

arising  from  other  focal  points  in  the  body,  it  can  not  be  rea- 
sonably argued  that  even  in  the  presence  of  partial  disorganiza- 
tion of  periapical  and  osseous  tissue  the  bacteria  necessary  to 
bring  about  an  acute,  subacute  or  chronic  inflammatory  process 
are  not  almost  always  available  in  sufficient  numbers.  As  a  pos- 
sible means  of  lessening  postoperative  complications  in  root  canal 
work,  the  use  of  milder  concentrations  of  germicidal  agents  is 
suggested,  so  graded  as  to  employ  in  the  neighborhood  of  the  peri- 
apical tissues  the  weakest  possible  solution  compatible  with 
germicidal  efficiency. 

Any  form  of  irritation  or  any  abnormal  degree  of  pressure  at 
the  gingival  margin  or  apex  of  the  root,  may  give  rise  to  non- 
septic  pericementitis.  It  also  results  frequently  upon  extirpa- 
tion of  the  pulp  and  is  due  in  such  an  instance  to  the  tearing 
of  the  pulp  from  its  connection,  with  the  formation  of  thrombi, 
and  to  extravasation  of  blood  into  the  apical  peridental  mem- 
brane. The  nonseptic  inflammation  which  thus  develops,  trans- 
lated clinically  as  pain  or  tenderness,  will  persist  until  such  time 
as  the  coagula  will  have  been  taken  care  of  by  mononuclear 
leucocytes.  "When  anesthetizing  the  pulp  by  the  cocain  pressure 
method  the  blood  content  of  the  pulp  is  partly  driven  into  the 
vessels  of  the  peridental  membrane  and  this  together  with  the 
formation  of  thrombi  resulting  from  the  extirpation  of  the  pulp 
brings  about  not  infrequently  a  painful  complication  in  the  shape  of 
a  nonseptic  pericementitis.  This  is  assuming,  of  course,  that  bac- 
teria have  not  invaded  the  periapical  tissues,  but  that  they  do  is, 
however,  the  case  more  frequently  than  the  former.  In  the  case 
of  teeth  devitalized  by  means  of  arsenic,  if  the  arsenical  applica- 
tion be  not  correctly  gauged,  its  absorption  into  the  pericemental 
tissues  will  give  rise  to  a  severe  nonseptic  pericementitis  which 
soon  thereafter,  however,  becomes  septic  in  character.  Another 
source  of  apical  traumatic  nonseptic  pericementitis  is  to  be  found 
in  frequent  and  unnecessary  manipulations  with  root  canal  in- 
struments in  the  neighborhood  of  the  apical  foramen,  and  the 
forcing  of  root  fillings  beyond  the  apical  foramen. 

If  the  cause  or  causes  of  a  nonseptic  inflammation  of  the  peri- 
dental membrane  should  persist,  in  time  the  result  will  be  the 
development  of  the  septic  form  of  pericementitis.  In  the  case 
of  the  apical  form  of  nonseptic  pericementitis  a  dentigerous  cyst 


NONSEPTIC    PERICEMENTITIS  411 

may  be  the  ultimate  result.  It  is  no1  an  infrequenl  occur- 
rence for  the  area  of  nonseptic  inflammation  in  the  peridental 
membrane  to  become  infected  by  microorganisms  which  gain  ac- 
cess to  ii  via  the  circulation.  The  accidental  perforation  of  a 
root  with  a  drill  may  give  rise  to  a  uonseptic  pericementitis  even 
though  the  instrumenl  was  a  sterile  one.  This  is,  however,  rarely 
the  case,  and  instead  a  septic  pericementitis  results,  accompanied 
by  the  absorption  of  an  area  of  cementum  and  of  dentin  im- 
mediately surrounding  the  perforation,  and  of  the  gum  tissue 
which  proceeds  until  the  area  of  absorption  is  completely  ex- 
posed at  the  gingiva.  The  passage,  accidental  or  intentional,  of 
root  canal  instruments  and  filling  materials  through  the  apical 
foramen,  only  rarely  results  in  a  nonbacterial  inflammation.  The 
lowering  of  the  vital  resistance  of  the  periapical  tissues  conse- 
quent upon  a  continued  irritation,  chemical  or  mechanical,  soon 
results  in  their  invasion  by  bacterial  forms. 


CHAPTER  XXXI 

SEPTIC  PERICEMENTAL  INFLAMMATION  AND  ACUTE 
AND  CHRONIC  DENTOALVEOLAR  ABSCESS 

Septic  pericemental  inflammation  may  be  acute  or  chronic  and 
is  caused  by  the  presence  in  1  lie  periapical  tissues  of  microor- 
ganisms which,  in  the  vast  majority  of  instances,  have  gained 
access  to  that  territory  via  the  root  canal.  If  the  bacteria  are  in 
sufficient  numbers  and  their  virulence  is  relatively  high,  and  if, 
on  the  other  hand,  the  resistance  of  the  individual  and  particu- 
larly of  the  invaded  tissue  cells  is  unequal  to  the  task  of  success- 
fully combating  the  invasion,  an  acute  dentoalveolar  abscess  will 
in  all  probability  result.  If  the  reverse  should  obtain,  the  dis- 
turbance in  the  peridental  membrane  will  be  slight,  and  the  in- 
fection will  be  overcome  with  no  permanent  injury  to  the  peri- 
dental membrane.  In  such  a  case  the  bacteria  will  be  destroyed 
by  the  polymorphonuclear  leucocytes  with  horseshoe-shaped  or 
partite  nuclei.  The  small  destruction  of  peridental  fibers  will 
be  replaced  by  cells  which  proliferate  from  the  preexisting  fixed 
fibers  of  the  membrane,  while  the  unaffected  leucocytes  will  enter 
the  lymph  stream  in  the  perivascular  lymph  spaces,  and  the  dead 
leucocytes  and  fixed  tissue  cells  will  be  carried  away  in  a  similar 
manner.  In  other  words,  the  bacteria  having  been  disposed  of 
and  their  toxins  neutralized,  a  repair  of  the  limited  destruction 
of  cells  takes  place  and  conditions  return  to  normal. 

If  the  invading  bacteria  are  of  low  virulence  from  the  begin- 
ning, or  following  the  subsidence  of  an  acute  dentoalveolar  ab- 
scess, a  chronic  dentoalveolar  abscess  will  result,  provided,  of 
course,  that  the  defensive  forces  of  the  body  are  unable  to  cope 
with  the  situation.  As  explained  later  in  this  chapter,  all  in- 
fections of  the  peridental  membrane  via  the  root  canal  do  not 
result  in  the  formation  of  abscesses,  acute  or  chronic.  It  is  for 
this  reason  that  the  title  of  this  chapter  specifies  pericemental  in- 
fection and  acute  and  chronic  dentoalveolar  abscess.  The  pres- 
ence of  pyogenic  bacteria  in  the  apical  region,  while  leading 
in  most  cases  to  the  formation  of  a  dentoalveolar  abscess,  never- 

412 


SEPTIC    PERICEMENTAL    INFLAMMATION  413 

theless,  in  some  few  eases,  cither  because  of  an  optimum  of  de- 
fensive forces,  or  of  timely  preventive  measures  (so-called  abor- 
tive measures  measures  intended  to  reestablish  a  normal  cir- 
culation in  the  area),  the  infection  in  the  periapical  tissues  does 
not  advance  to  the  stage  of  visible  pus  formation  with  involve- 
ment of  the  adjacent   cancellated  bone  of  the  jaw. 

A  pulp  may  be  the  sent  of  suppuration,  of  putrefaction,  or  of 
suppuration  followed  by  putrefaction.  It  is  well  to  remember, 
therefore,  thai  a  "decomposed"  or  so-called  "putrescent  pulp" 
is  the  result  of  a  suppurative  process,  followed  in  a  large  num- 
ber of  instances  by  putrefactive  changes;  or  it  may  be  the  re- 
sult of  purely  putrefactive  changes.  Suppuration  is,  of  course. 
the  result  of  the  infection  of  a  tissue — in  this  instance  the  dental 
pulp,  by  pyogenic  and  other  organisms,  whose  toxins  are  capa- 
ble of  causing  degenerative  changes  and  liquefaction  of  tissue 
cells.  The  remains  of  the  dead  cells  and  the  extravasated  serum 
offer  excellent  pabulum  for  that  kind  of  bacteria  (saprophytic) 
which  thrive  upon  dead  or  disorganized  tissue.  Saprophytic  bac- 
teria gain  access  to  the  tissue  previously  disorganized  and  de- 
vitalized by  the  activity  of  the  pyogenic  bacteria;  or  else  it  is 
possible  that  the  pyogenic  cocci,  and  others  among  the  original 
bacterial  exciters,  have  in  themselves  the  power  of  further  split- 
ting the  dead  nitrogenous  matter;  viz.,  the  dead  cells  of  the  pulp 
and  the  dead  wandering  cells.  The  end  products  of  the  suppura- 
tive process  are  in  this  way  further  broken  down.  The  simplifi- 
cation of  dead  nitrogenous  matter  by  the  activity  of  saprophytic 
microorganisms  is  termed  putrefaction. 

Basic  cadaveric  alkaloids,  or  ptomaines,  are  produced  by  the 
decomposition  of  this  dead  nitrogenous  matter,  through  the 
agency  of  saprophytic  organisms.  Cadaverin,  putrescin,  neuridin, 
neurin,  and  methyl  guanidin  are  some  of  the  most  important.1 

In  the  study  of  pericemental  infections,  we  should  constantly 
bear  in  mind  that  the  products  of  nitrogenous  decomposition  are 
in  themselves  capable  of  inciting  an  inflammatory  process.  When 
particles  of  a  pulp  which  has  been  the  seat  of  suppuration  and 
subsequent  putrefaction,  or  of  putrefaction  alone,  are  forced 
through  the  apical  foramen  accidentally  or  in  the  course  of  de- 
fective root  canal  technic,  an  acute  infection  may  develop  in  the 


1Ziegler:     General   Pathology,   New   York,  Win.   Wood  &  Co. 


414  DENTAL   PATHOLOGY 

periapical  tissues  within  twenty-four  hours  thereafter.  It  is 
probable  that  the  activity  of  the  process  is  due  not  only  to  the 
forcing  of  pyogenic  organisms  through  the  apical  foramen,  and 
to  a  change  in  the  oxygen  tension  in  the  root  canal  and  peri- 
apical tissues,  which  confers  increased  virulence  to  the  faculta- 
tive anaerobic  bacteria  in  the  periapical  tissues,  but  also  to  the 
presence  therein  of  some  of  the  cadaveric  alkaloids  above  men- 
tioned although  this  latter  is  not  the  most  important  contin- 
gency. The  organic  contents  of  the  dentinal  tubules,  viz.,  den- 
tinal fibrillar  and  their  ramifications,  are,  of  course  also  subject  to 
putrefactive  changes.  According  to  Vaughan  and  Xovy,  ca- 
daverin  and  putrescin  are  capable  of  producing  strong  inflam- 
mation and  necrosis.  In  large  doses  they  are  poisonous  to  mice, 
rabbits,  and  guinea  pigs.  Cadaverin  lias  been  found  to  produce 
suppuration  in  the  absence  of  bacteria;  neuridin  is  one  of  the 
most  common  products  of  putrefaction,  and  while  it  is  not  poi- 
sonous in  itself,  it  develops  a  toxic  action  when  in  association 
with  other  products  of  putrefaction.2 

Neurin,  however,  which  occurs  in  the  putrefaction  of  human 
flesh  is  in  itself  a  highly  poisonous  alkaloid. 

In  by  far  the  larger  percentage  of  cases  the  apical  section  of 
the  peridental  membrane  is  the  one  first  to  be  attacked  by  in- 
fection via  the  root  canal.  These  involvements  of  the  pulp  are 
the  immediate  consequence  of  neglected  dental  caries  and  in 
the  absence  of  the  latter  disease  it  is  safe  to  assume  that,  ex- 
cepting a  negligible  percentage  of  cases,  septic  apical  perice- 
mentitis would,  of  course,  not  develop.  The  importance  of  pre- 
venting the  onset  and  progress  of  dental  caries  is  the  key  to 
the  prevention  of  septic  infections  of  the  apical  peridental  mem- 
brane, and  of  dentoalveolar  abscess,  either  acute  or  chronic. 

Prophylaxis  of  Pulp  Involvements 

Dental  caries  is,  to  a  large  extent,  a  preventable  disease,  and 
the  secret  of  its  prevention  lies  in  the  thoroughness  and  per- 
sistence with  which  the  prevailing  methods  of  prophylaxis  are 
carried  out.  While  the  constitutional  factor  in  dental  caries  un- 
doubtedly influences  the  extensiveness  and  rapidity  of  the  proc- 
ess, it  does  so,  however,  only  in  a  small  proportion  of  cases. 


2 Vaughan   and   Xovy: 


SEPTIC    PERICEMENTAL    INFLAMMATION  415 

What  these  constitutional  predisposing  causes  are  we  arc  un- 
able to  state  with  any  degree  of  definiteness.  Theories  have  been 
promulgated  here  and  there  in  the  effort  to  blaze  the  way  to- 
ward a  reasonable  solution  of  the  problem,  but  as  yet  nothing 
bearing  the  stamp  of  scientific  conviction  has  been  adduced.  The 
influence  of  the  mineral  constituents  of  drinking  water,  the  na- 
ture of  the  food  used,  climate,  soil,  the  influence  of  the  internal 
secretions,  the  elaboration  within  the  body  and  the  secretion 
within  the  oral  cavity  of  substances  capable  of  being  split  into 
compounds  having  solving  properties  on  the  enamel  of  the  teeth, 
are  some  of  the  factors  which  have  been  discussed  as  having  a 
possible  bearing  upon  the  prevalence  of  dental  caries.  But  after 
all,  about  the  only  phases  of  the  problem  of  caries  prevention 
about  which  accurate  data  are  available  are  the  actual  steps 
of  its  production  beginning  with  the  dissolution  of  the  conti- 
nuity of  the  enamel  prisms  by  lactic  acid.  In  other  words, 
while  we  know  the  steps  in  the  process  of  caries,  we  are  in  ob- 
scurity regarding  the  underlying  factors  or  conditions  which 
bring  about  caries,  rapid  or  slowr  progressing,  or  which  determine 
an  immunity  or  nonsuseeptibility  to  this  disease. 

Therefore,  in  the  work  of  caries  prophylaxis  all  measures  are 
generally  aimed  at  the  ultimate  causes  responsible  for  its  onset — 
causes  of  a  purely  local  character  and  preventable  in  most  cases. 
The  continuous  supervision  of  patients  from  the  time  of  the  erup- 
tion of  the  deciduous  teeth,  with  the  view  of  maintaining  the 
surfaces  of  the  teeth  in  a  condition  of  strict  cleanliness,  and  to 
insure  correct  occlusion  of  their  permanent  successors;  the  oc- 
casional treatment  of  the  fissures  of  the  molars  with  silver  nitrate, 
if  supplemented  by  the  thorough  brushing  of  the  teeth  upon  ris- 
ing, after  each  meal,  and  upon  retiring,  will  greatly  reduce  the 
prevalence  of  caries.  And  ipso  facto  the  involvement  of  the  pulp, 
its  death  by  suppuration  or  putrefaction  or  both,  and  the  spread- 
ing of  the  infectious  process  to  the  peridental  tissues,  will  like- 
wise be  circumvented. 

Etiology  of  Septic  Apical  Pericementitis 

The  causes  of  septic  apical  pericementitis  may  be  enumerated 
as  bacteria  and  bacterial  products  which  have  invaded  the  peri- 
apical  tissues  proceeding  from  the  root  canal  inwardly  (Figs. 


416 


DENTAL   PATHOLOGY 


329-334).  They  are  a  combination  of  the  pyogenic  organisms 
■which  have  been  instrumental  in  destroying  the  pulp,  and  the 
saprophytic  organisms  which  may  follow  in  their  wake;  and  to 
these  must  be  added  the  products  of  nitrogenous  decomposition. 
The  peridental  membrane  is  infected  by  continuity  from  the  in- 


Fig.  329. — Chronic  dentoalveolar  abscess 
of  an  upper  lateral  incisor  with  a  large 
area  of  rarefaction.  The  infectious  proc- 
ess involved  an  adjacent  tooth  on  each 
side.  An  incompletely  tilled  root  canal 
was  evidently  the  cause  of  the  continued 
infection. 


Fig.  330. — Chronic  dentoalveolar  ab- 
scess, in  a  lower  right  first  molar  involving 
both  roots.  The  source  of  the  infection 
was  the  incompletely  treated  and  filled  root 
canals. 


Fig.  331. — Chronic  dentoalveolar  ab- 
scess involving  the  upper  first  and  second 
left  bicuspids.  The  apical  portion  of  the 
root  of  the  second  bicuspid  has  undergone 
absorption. 


Fig.  332. — Three  chronic  dentoalveolar 
abscesses  in  connection  with  upper  right 
first  and  second  bicuspids  and  first  molar. 
The  root  canals  were  the  source  of  the  in- 
fection. 


fection  in  the  root  canal.  It  may  also  become  the  seat  of  an  in- 
flammation following  the  passage  through  the  apical  foramen  of 
the  saprophytic  bacteria  with  the  products  of  their  activity, 
■which  were  concerned  in  the  decomposition  of  a  pulp  which  has 


SEPTIC    I'KKICKMKNTAL    INFLAMMATION 


417 


succumbed  following  the  infliction  of  a  traumatism,  such  as  a 
blow  or  the  sudden  impact  upon  a  hard  substance  in  1  lie  course 
of  mastication,  or  the  continued  action  of  thermal  irritation  in  the 

absence  of  external  opening  in  the  crown.  Occasionally  even  in 
the  absence  of  dental  caries,  saprophytic  infection  of  the  pulp 
occurs  either  via  the  blood  stream  (i.  e.,  blood  vessels  of  the 
apical  peridental  membrane),  or  through  imperfections  in  the 
enamel.  In  the  latter  instance,  the  process  has  been  compared  by 
Inglis3  to  the  putrefactive  decomposition  of  eggs  in  the  presence 
of  apparently  unbroken  shells.  The  putrefactive  process  spread- 
ing from  the  pulp  into  the  periapical  tissues  doubtless  plays  an 


Pig.  333. — Chronic  dentoalveolar  ab- 
scess in  upper  first  and  second  bicuspid. 
The  root  canals  were  the  source  of  the  in- 
fection. 


Fig.  334. — Chronic  dentoalveolar  ab- 
scesses in  upper  first  bicuspid  and  second 
molar.  The  path  of  the  periapical  infec- 
tion in  the  molar  has  joined  with  an  in- 
fection also  chronic  which  originated  at 
the    gum    margin. 


indirect  role  in  the  development  of  an  acute  suppuration.  There 
follows  a  decrease  in  the  vital  resistance  of  the  periapical  tis- 
sues, and  a  subsequent  infection  by  pyogenic  organisms  which 
reach  the  area  by  way  of  the  blood  stream;  or,  the  bacteria  re- 
sponsible for  the  putrefactive  decomposition  consist  of  varieties 
among  which  some  assume  parasitic  powers  by  a  change  of  en- 
vironment from  a  disorganized  to  a  living  medium.  At  any  rate, 
the  passage  of  the  bacteria  concerned  in  the  decomposition  of  a 
dead  pulp,  and  of  the  animal  alkaloids  to  which  they  give  rise, 
is  soon  followed  in  the  periapical  tissues  by  suppuration  and 
dentoalveolar  abscess  formation. 


3Inglis-Burchard:      Dental    Pathology. 


418 


DENTAL   PATHOLOGY 


The  etiology  of  periapical  infection  is  not,  however,  limited  to 
preexisting  infections  in  the  root  canal  resulting  from  suppura- 
tion or  putrefaction  of  the  pulp,  or  of  a  combination  of  both  proc- 
esses. In  a  number  of  cases  after  extirpation  of  a  noninfected 
pulp  the  periapical  tissues  become  the  seat  of  an  infectious  in- 
flammation. The  infection  in  these  instances  has  been  carried 
beyond  the  apical  foramen  by  unsterile  instruments  or  dressing 
cotton,  or  by  failure  to  properly  protect  the  root  canal  by  means 
of  the  rubber  dam  against  contamination  from  the  saliva. 


F" 


*• 


d 


Fig.  335. — Chronic  dentoalveolar  ab- 
scess involving  the  roots  of  the  upper  left 
second  bicuspid  and  upper  left  first  molar. 
The  roots  did  not  penetrate  the  maxillary 
sinus  as  might  be  surmised  from  the  pic- 
ture and  the  maxillary  sinus  was  not  af- 
fected. The  infectious  process  involved 
the  osseous  tissue  of  the  maxilla  anterior 
to  the  external  wall  of  the  maxillary  sinus. 


Fig.  336. — Chronic  dentoalveolar  abscess 
involving  the  upper  right  central  and  lateral 
incisors.  The  chronic  osteomyelitis  resulted 
in  caries  of  bone  over  a  relatively  large 
area.  Fully  two-thirds  of  the  lateral  incisor 
projected  into  this  cavity. 


Again,  the  periapical  tissues  may  become  the  seat  of  an  infec- 
tion by  continuity  from  an  infection  in  an  adjoining  tooth  (Figs. 
335,  33G  and  337).  It  is  not  at  all  rare  to  find  that  one  or  two 
adjoining  teeth  on  either  side  of  the  primarily  infected  periapical 
peridental  membrane  have  become  involved.  The  infectious  proc- 
ess spreads  through  the  cancellated  spaces  to  an  adjoining  tooth 
and  from  there  it  may  involve  one  or  two  teeth  more.  Infec- 
tion of  the  peridental  membrane,  with  acute  dentoalveolar  ab- 
scess formation  as  the  consequence,  may  also  occur  from  an  in- 
fection which,  beginning  at  the  gum  margin,  advances  toward  the 
apical  region.  Here  the  infection  involves  the  pulp  which,  how- 
ever, does  not  succumb  at  once  in  all  instances.    One  of  this  type 


SEPTIC    PERICEMENTAL    [NFLAMMATION  410 

of  cases  showed  n  wel L-ma rke.l  area  of  ra re l';iet inn  in  the  apical 
region,  and  when  examined  clinically  by  percussion,  gave  every 
indication  of  being  the  seal  of  a  chronic  dentoalveolar  abscess. 
The  tooth  was  opened  into,  bu1  ool  before  having  to  resort  to 
novocaine  anesthesia,  much  to  the  intense  surprise  of  the  operator 
and  the  discomforl  of  the  patient.  The  pulp  was  removed  and 
this  was  followed  by  a  discharge  of  pus.  The  pulp  had  main- 
tained its  vitality  in  spite  of  the  suppurative  process  in  the  peri- 
apical region,  probably  through  an  attenuated  connection  with 
its  source  of  blood  and  nerve  supply. 

Septic  pericementitis,  acute  or  chronic,  is  also  caused  by  per- 
forations of  the  walls  of  root  canals  by  drills,  burs,  etc.,  (Figs. 
338-339),  or  by  the  passage  through  the  apical  foramen  of  in- 
fected broaches  or  drills  (Fig.  340).    A  chronic  infection  is  usu- 


Kig.  337. — Chronic  dentoalveolar  abscess  (so-called  dental  granuloma)  in  connection 
with  an  upper  left  first  and  second  bicuspid.  By  a  process  of  continuity  the  infection 
spread   to   the   mesio-buccal    root   of   the   adjoining  first   molar. 

ally  the  result,  located  on  the  lateral  aspect  of  the  single-rooted 
teeth  and  in  the  bifurcation  of  bicuspids  and  the  trifurcation  of 
molars.  In  some  instances  the  alveolar  process  and  the  gum  tis- 
sue from  the  gingival  margin  to  the  perforation  disappear  (fol- 
lowing the  infection  of  the  perforated  area  of  the  peridental 
membrane)  to  the  level  of  the  perforation,  exposing  that  much 
of  the  root  surface.  Several  such  eases  have  come  under  our  ob- 
servation. 

Another  interesting  cause  of  alveolar  abscess  is  intraalveolar 
root  fractures,  caused  by  external  severe  traumatisms  (Fig.  341). 
We  have  recently  observed  two  such  cases.  One  of  them  was  in  a 
young  acrobat,  who  presented  upon  the  gum  between  the  upper 
left  central  and  lateral  incisors  a  sinus  one  inch  in  length  parallel 


420 


DENTAL   PATHOLOGY 


to  the  long  axis  of  the  face.  The  alveolar  infection  was  of  long 
duration  and  had  been  brought  about  by  the  intraalveolar  frac- 
ture of  the  root  of  the  lateral  incisor,  following  presumably  an 
effort  to  lift  with  his  teeth  some  extraordinary  weight.  The  in- 
fection became  apparent  years  after  the  accident.    At  times  con- 


Fig.  338. — Chronic  dentoalveolar  abscess  in  the  Fig.    339. — Chronic  dentoalveolar 

bifurcation    of    the    roots    of    the    lower    right    first  abscess  caused  by  the  perforation  of 

molar    brought    about    by    the    perforation    of    the  the   distolingual   aspect    of   an   upper 

mesial   wall   of  the  posterior   root.  second  bicuspid. 


Fig.  340. — Chronic  dentoalveolar  ab- 
scess caused  by  a  fragment  of  a  broach 
broken    in   the    root   canal. 


Fig.  341. — Intraalveolar  root  fracture 
of  an  upper  right  cuspid,  which  caused  a 
chronic  infection  of  long  standing.  The 
destructive  inflammation  had  produced  a 
sinus  whose  course  was  through  the  labial 
alveolar  plate. 


ditions  would  be  quiet,  at  others  a  discharge  would  take  place 
from  the  sinus.  When  examined  by  the  writer  the  fragment  of 
root  was  found  at  the  mouth  of  the  sinus,  and  was  removed 
with  a  pair  of  dressing  pliers.  The  other  case  was  that  of  a 
woman  giving  no  history  of  traumatism,  but  having  suffered  in- 
tensely from  "an  abscess  in  one  of  her  upper  teeth."     Two  or 


SEPTIC    PERICEMENTAL    INFLAMMATION-  421 

three  teeth  posterior  to  the  upper  left  cuspid  had  been  extracted 
to  remedy  ;i  condition  brought  about  by  the  intraalveolar  frac- 
ture of  the  upper  left  cuspid.  The  extraction  of  the  fractured 
tooth,  as  expected,  resulted  in  the  disappearance  of  all  symptoms 
of  infection. 

The  foregoing  causes  may  he  summarized  as  follows: 

1.  Through  the  root  canal  or  canals,  by  a  process  of  continuity. 
following  suppuration  or  putrefaction  or  both  as  the  result  of 
deep-seated  dental  caries. 

2.  Following  death  of  the  pulp  by  traumatisms  or  thermal  irri- 
tation, in  the  absence  of  caries  or  any  break  in  the  continuity  of 
the  hard  tissues  of  the  crown  but  with  the  development  of  pu- 
trefactive processes  in  the  dead  pulp. 

3.  Following  the  extirpation  of  a  healthy  pulp  (preliminary  ab- 
sence of  infection  in  canal  contents),  the  infection  being  carried 
to  the  periapical  peridental  membrane  in  the  course  of  canal  in- 
strumentation, or  because  of  insufficient  protection  against  con- 
tamination from  the  saliva. 

4.  By  continuity  from  an  infection  in  an  adjoining  tooth  or 
teeth. 

5.  By  continuity  from  an  infection  of  the  gingivae  the  peri- 
apical tissues  become  infected  and  a  dentoalveolar  abscess  fol- 
lows. This  source  of  infection  may  also  give  rise  to  pathologic 
reactions  in  the  peridental  membrane  of  the  pyorrhea  alveolaris 
type.  A  paroxysmal  intensification  of  the  infection  which  orig- 
inates in  the  gingival  margin  results  in  a  form  of  abscess  of  the 
investing  tissues  known  as  "pyorrhea  abscess"  or  "lateral  ab- 
scess." 

6.  Through  accidental  perforation  of  the  floor  of  the  pulp 
chamber  or  wall  of  a  root  canal. 

7.  As  the  result  of  intraalveolar  root  fracture. 

Periapical  Infection  by  the  Hematogenic  Route 

Bacteria  may  reach  the  periapical  tissues  by  way  of  the  circu- 
lation and  become  active  in  some  area  of  the  periapical  tissues 
or  some  other  section  of  the  peridental  membrane  previously 
weakened  by  mechanical  or  chemical  irritation.  This  mode  of  in- 
fection of  the  peridental  membrane,  while  not  of  frecpaent  oc- 
currence, is  nevertheless  not  to  be  overlooked. 


122  DENTAL   PATHOLOGY 

There  is  as  much  Logic  in  assuming  that  foci  of  chronic  infec- 
tion upon  areas  of  the  body  at  remote  distances  from  the  teeth 
and  jaws  may  bring  about  infections  of  the  peridental  memhrane, 
as  there  is  in  accepting  the  possibilities  of  metastatic  infections 
from  foci  of  infection  around  or  upon  the  roots  of  teeth.  The 
--'•ailed  pericemental  abscess,  first  discussed  by  D.  D.  Smith, 
and  subsequently  minutely  investigated  by  Kirk  and  Darby,  is 
a  possible  instance  of  infection  of  the  peridental  membrane  via 
the  blood  stream.  It  is  of  course  admitted  that  the  infection  in 
these  pericemental  abscesses  in  teeth  having  live  pulps  may  also 
originate  at  the  gum  margin,  but  the  clinical  evidence  in  the 
cases  described  by  Kirk  points  with  more  definiteness  toward  the 
hematogenic  mode  of  invasion.  The  lateral  or  pyorrheal  abscess 
is  a  pathologic  reaction  different  from  the  pericemental  abscess, 
and  is  the  result  of  either  an  exacerbation  of  an  infection  in  the 
soft  tissue  of  the  gum.  the  bacteria  having  penetrated  through 
the  subgingival  space,  or  else  of  the  infection  through  the  epi- 
thelium of  the  gum  tissue  overlying  the  pyorrhea  pocket  when 
the  gingiva  has  been  previously  destroyed  by  the  infection. 

Recovery  from  Periapical  Infections.     Acute  and  Chronic 

Processes 

Septic  apical  pericementitis  does  not  lead  in  every  case,  as  pre- 
viously stated,  to  the  formation  of  an  acute  or  chronic  dento- 
alveolar  abscess.  In  those  instances  in  which  the  invading  or- 
ganisms are  of  low  virulence  and  are  present  in  relatively  small 
numbers,  and  when  the  vital  resistance  of  the  invaded  tissue  cells 
is  high,  the  symptoms  of  the  inflammatory  process  subside  be- 
fore reaching  the  stage  of  abscess  formation.  Again,  it  should  be 
noted  that  the  periapical  tissues  may  be  invaded  by  bacteria 
which  from  the  start  give  rise  to  chronic  symptoms.  For  in- 
stance, following  the  extirpation  of  a  normal  pulp,  if  every  step 
of  the  operation  has  not  been  performed  with  regard  to  complete 
asepsis  there  will  develop  in  twenty-four  to  forty-eight  hours 
symptoms  of  periapical  pericementitis.  This  inflammation  is  in 
many  cases  due  to  the  introduction  of  bacteria  into  the  peri- 
apical tissues  in  the  course  of  instrumentation. 

These  forms  of  septic  apical  pericementitis  do  not  always  pro- 
gress to  abscess  formation.     One  or  two  conditions  account  for 


SEPTIC    PERICEMENTAL    INFLAMMATION  123 

the  subsidence  of  the  symptoms.  The  infection  is  either  entirely 
overcome  by  the  natural  defenses  of  the  body,  or  else  all  of  the 
bacteria  are  qo1  overcome;  and  then,  being  of  Low  virulence,  re- 
main  in  the  periapical  tissues  and  se1  up  a  low  grade  inflamma- 
tion, thus  establishing  a  chronic  periapical  abscess  a  so-called 
blind  abscess  or,  erroneously  a  dental  granuloma,  encapsulated 
by  a  Avail  of  fibrous  tissue.  In  the  former  ease  (viz.,  when 
the  infection  is  overcome  following-  active  phagocytosis)  it 
is  to  be  assumed  thai  the  bacteria  have  caused  recoverable  cell 
degeneration  or.  at  most,  the  death  of  so  few  cells  thai  their  re- 
placement by  new  cells  through  the  agency  of  fibroblasts  is 
readily  accomplished. 


CHAPTER  XXXII 

ACUTE  APICAL  DENTOALVEOLAR  ABSCESS 

The  infection,  if  it  progresses  to  the  point  of  acute  clento- 
alveolar  abscess  formation  in  the  periapical  tissues,  because  of  the 
high  virulence  of  the  bacteria  and  their  presence  in  large  num- 
bers, together  with  the  low  resistance  of  the  invaded  tissue  cells, 
advances  through  the  alveolar  bone  to  discharge  at  some  point 
in  the  mouth,  or  on  the  face,  or  neck,  and  in  rare  instances  in 
areas  of  the  body  even  more  remote  from  the  original  seat  of  the 
infection. 

An  acute  apical  dentoalveolar  abscess  may  be  defined  as  an  area 
of  infection  localized  in  the  apical  region  of  the  peridental  mem- 
brane, originating  in  the  vast  majority  of  cases  in  a  preexisting- 
infection  in  a  root  canal  or  canals  of  the  corresponding  tooth, 
and  in  a  few  instances  from  a  previously  infected  apical  area 
of  a  neighboring  peridental  membrane.  It  is  at  first  but  poorly 
circumscribed.  It  develops  as  readily  upon  deciduous  as  upon 
permanent  teeth  and  is  in  the  majority  of  cases  the  sequela  of 
neglected  dental  caries.  In  multirooted  teeth  the  pulp  in  one, 
and  even  in  two  root  canals  may  be  alive,  while  in  the  remain- 
ing root  canal  it  may  have  undergone  suppuration  or  putrefac- 
tive decomposition,  or  both,  involving  the  apical  peridental  mem- 
brane and  resulting  in  an  acute  dentoalveolar  abscess. 

Such  an  abscess  shows  at  first  evidences  of  being  slightly  cir- 
cumscribed. The  virulence  of  the  infection — the  rapidity  with 
which  the  bacterial  toxins  destroy  the  cells  with  which  they  come 
into  contact,  either  directly  or  indirectly — prevents  to  some  ex- 
tent that  form  of  tissue  proliferation  which  eventually  results  in 
the  encapsulation  of  a  focus  of  infection.  Tissue  proliferations 
are  in  inverse  ratio  to  the  virulence  of  the  infection,  the  less 
virulent  the  infection,  the  more  abundant  the  tissue  prolifera- 
tions ;  and  vice  versa. 

From  a  pathologic  standpoint  the  chronicity  or  acuteness  of  an 
inflammation  is  not  determined  exclusively  by  the  relative  de- 
gree of  virulence  of  the  bacteria,  or  the  severity  of  the  symp- 

424 


ACTTTE   APICAL   DENTOALVEOLAR    ABSCESS  425 

toms,  or  the  time  consumed  by  the  infectious  process  up  to  the 
establishment  of  a  sinus.  An  inflammation  is  chronic  when  the 
amount  of  connective  tissue  of  repair  (fibroblasts)  predominates, 
and  "when  among  the  leucocytes  which  have  been  called  to  the 
seat  of  the  infection  the  mononuclear  variety  predominates;  it 
is  acute  when  the  fibroblasts  and  the  fibers  to  which  they  give 
origin  are  in  the  minority  and  the  polymorphonuclear  leucocytes 
are  in  the  majority.  In  chronic  inflammations  the  mononuclear 
leucocytes  and  plasma  cells  are  in  the  majority,  while  in  the  acute 
inflammations  the  polymorphonuclear  leucocytes  are  in  the  ma- 
jority. 

Clinical  Symptoms 

The  symptoms  accompanying  the  development  and  progress 
of  an  acute  apical  alveolar  abscess  are: 

1.  Tenderness  of  the  tooth  to  percussion  and  upon  mastication. 

2.  Pain. 

3.  Swelling. 

4.  Increased  redness  of  the  gum  overlying  the  affected  tooth 
and  adjacent  areas. 

5.  Tenderness  on  pressure  on  the  gums  over  the  apical  region 
of  the  tooth. 

6.  Looseness  and  protrusion  of  the  tooth. 

7.  Rise  in  temperature. 

8.  Constipation. 

9.  Fetor  of  breath. 

10.  General  malaise. 

11.  Headache. 

The  pain,  slight  at  first,  increases  gradually  in  severity;  it  is 
throbbing  in  character  and  is  intensified  upon  assuming  a  re- 
clining position  and  does  not  begin  to  subside  until  the  im- 
prisoned inflammatory  exudates,  liquid  and  solid,  reach  the  soft 
tissues  overlying  or  underlying  the  affected  tooth.  Tenderness 
to  pressure  is  in  all  instances  indicative  of  inflammation  of  the 
peridental  membrane  and  the  greater  the  area  of  peridental  mem- 
brane involved  the  more  pronounced  the  tenderness.  In  severe 
inflammations  of  the  pulp,  it  might  be  remarked  in  passing,  either 
septic  or  nonseptic,  the  periapical  tissues  become  likewise  in- 
volved in  the  inflammatory  process  and  thus,  even  in  the  pres- 


426  DENTAL   PATHOLOGY 

enee  of  a  vital  pulp,  a  painful  response  to  percussion  may  occur. 
This  tenderness  is  in  response  to  stress  of  occlusion  or  to  per- 
cussion of  the  tooth  for  diagnostic  purposes.  Pain  is  also  due 
to  an  exaggerated  intraosseous  pressure,  the  inflammatory  ex- 
udates, liquid  and  solid,  being  enclosed  in  the  cancellated  spaces, 
freely  supplied  with  blood  vessels  and  nerves.  Practically  all 
acute  dentoalveolar  abscesses,  if  proper  measures  are  not  in- 
stituted to  remove  all  sources  of  infection  in  the  root-canal,  be- 
come in  time  chronic. 

The  protrusion  of  a  tooth  is  caused  by  infiltration  of  the  peri- 
dental membrane  by  inflammatory  liquid  and  solid  exudates  (leu- 
cocytes), and  by  the  swelling  of  the  cells  of  the  peridental  mem- 
brane— the  cloudy  or  hydropic  degeneration  which  accompanies 
inflammation  in  connective  tissue.*  In  the  acute  form  of  dento- 
alveolar abscess  there  is,  as  a  general  rule,  comparatively  little 
destruction  of  peridental  fibers,  and  consequently  these  teeth 
frequently  recover  following  correct  instrumental  and  therapeutic 
technic  and  the  filling  of  the  root  canals,  previously  rendered 
aseptic,  to  the  apex. 

With  the  increase  of  intraosseous  pressure  there  is  an  increase 
of  pain,  increased  blood  pressure,  and  a  rise  in  temperature  of 
from  one  to  four  degrees  F.  The  tongue  is  thickly  furred,  the 
breath  offensive,  and  the  patient  shows  evidences  of  toxemia. 
From  twelve  to  thirty-six  hours,  but  in  some  cases  longer,  after 
the  pain  becomes  well  marked,  the  infectious  process  has  pro- 
gressed through  the  cancellated  and  cortical  bone  and  estab- 
lished an  opening  through  the  latter.  The  inflammatory  exudate 
(serum,  lymph,  degenerated  and  dead  leucocytes  and  fixed-tissue 
cells)  is  now  under  the  periosteum,  and  after  the  infection  has 
brought  about  a  destruction  of  a  small  area  of  the  periosteum 
the  adjacent  soft  tissues  become  involved,  and  the  face  swells. 

The  gum  tissues  overlying  the  root  of  the  affected  tooth  appear 
red,  flabby,  and  swollen  from  the  beginning  of  the  infection, 
slightly  at  first,  but  increasingly  so  as  the  infection  progresses. 
The  extensive  swelling  of  the  tissues  of  the  mouth,  face  and  neck 
is  not  due  entirely  to  diffusion  of  pus  through  the  tissues,  be- 
cause edema  enters  largely  into  the  process.  The  cellulitis  is 
accompanied  by  difficulty  in  opening  the  mouth,  which  persists  for 
days  after  the  establishment  of  the  sinus.     But  the  difficulty  in 


*Adami  and  McCrae:     Texl    Book  of  Pathology,  Philadelphia,  Lea  and  Febiger. 


SlCUTE    APICAL    DENTOALVEOLAR    ABSCESS  1*2  i 

opening  the  mouth  is  due  qoI  only  to  the  distention  of  the  tis- 
sues by  swelling,  bu1  also  to  involvemenl  of  muscular  tissue,  par- 
ticularly of  the  masseter  and  buccinator  muscles,  which  for  the 
time  being  supplied  with  an  excess  of  stimulus  are  maintained 
in  ,i  semicontracted  state. 

Sinus  Formation 

The  course  of  a  sinus  from  a  dentoalveolar  abscess  is  governed 
by  the  location  of  the  affected  tooth,  upper  or  lower,  in  the  arch, 
the  density  of  the  tissues  overlying  the  seat  of  the  abscess,  the 
virulence  of  the  infection,  gravity,  and  the  injudicious  applica- 
tion of  hot  poultices  (Fig.  342).     Acute  dentoalveolar  absc< 

in  connection  with  the  upper  central  and  lateral  incisors  and 
cuspids  may  discharge  upon  the  labial  or  palatal  aspects  of  the 
maxilla,  but,  as  a  general  rule,  the  sinus  will  open  upon  the  ex- 
ternal, or  labial,  aspect.  Dentoalveolar  abscesses  in  connection 
with  the  lateral  incisor  and  palatal  root  of  the  first  molar  have 
occasionally  been  observed  to  discharge  upon  the  palatal  as- 
pect of  the  jaw.1 

Sinuses  from  dentoalveolar  abscesses  in  upper  single-rooted 
teeth  and  in  the  buccal  roots  of  multirooted  teeth  discharge,  as 
a  rule,  upon  the  labial  and  buccal  aspects,  respectively;  discharge 
upon  the  palatal  side  is  the  exception. 

Dentoalveolar  abscesses  in  connection  with  the  central  and 
lateral  incisors,  cuspids,  or  first  and  second  bicuspids,  may  dis- 
charge into  the  nasal  cavity,  the  sinus  opening  in  the  floor  of  that 
cavity.  An  abscess  upon  a  cuspid,  bicuspid,  first,  second  or  third 
molar,  may  discharge  into  the  maxillary  sinus.  The  shape,  size 
and  location  of  the  maxillary  sinus  vary  with  practically  each 
individual;  consequently,  the  relationship  of  the  upper  teeth  to 
that  cavity  varies  with  equal  frequency.  The  upper  cuspid,  and 
even  the  lateral  incisor,  have  been  known  to  produce  infection 
of  the  maxillary  sinus.2 

It  is  of  importance  to  note  that  bone  changes  are  not  always 
visible  in  cases  in  which  the  maxillary  sinus  has  become  involved 
by  continuity  from  an  infection  on  the  root  of  the  tooth.  It  has 
been  shown  by  Hunsberg  and  Hyjek  that  it  is  possible  to  have  an 


1Turner,   J.    G. :      In    Science   and   Practice   of  Dental    Surgery,   by   N.    G.    P.ennett. 
-Seydell,   E.    M  :     International  Journal  of  Orthodontia,   ii,   Xo.   6,   344. 


428 


DENTAL   PATHOLOGY 


extension  of  an  infection  through  the  Avails  of  the  frontal  and 
sphenoidal  sinus  to  the  neighboring  parts  without  macroscopic 
changes  in  the  bone.3 


Fig.    342. — Result   of  poulticing  the   face   in  connection   with   acute   dentoalveolar   abscesses 

(Oakman). 

It  is  rare  that  teeth  abutting  against  the  floor  of  the  antrum 
have  not  a  thin  lamina  of  bone  between  the  apices  of  the  roots 


3ibid. 


ACUTE   APICAL    DENTOALVEOLAR   ABSCESS  429 

and  the  mucoperiosteuni  of  the  sinus.  If  a  tooth  suspected  of 
being  the  cause  of  an  involvement  of  the  sinus  should  be  extracted 
and  no  opening  should  be  found  leading  into  the  sinus,  it  is  no 
evidence  thai  such  a  toot li  was  not  at  fault.  The  infectious  proc- 
ess may  have  established  a  microscopic  opening  undiagnosable 
by  instrumentation. 

Teeth  rarely  discharge  upon  the  lingual  aspect  of  the  mandible, 
because  of  the  greater  thickness  of  bone  between  the  apical  areas 
of  the  teeth  and  the  lingual  aspect  of  the  mandible,  than  toward 
the  labial  side.  A  dentoalveolar  abscess  in  connection  with  any 
one  of  the  lower  teeth  may  " point"  externally,  gravity  being 
to  some  extent  a  factor  in  deciding  upon  that  course  of  discharge. 
If  the  infection  has  followed  a  course  above  the  origin  of  tbe 
deep  cervical  fascia,  the  point  of  discharge  will  be  above  the 
lower  border  of  the  mandible  ;  but  if,  on  the  other  hand,  the  course 
of  the  infection  has  been  under  the  deep  cervical  fascia,  the  point 
of  discharge  may  be  somewhere  upon  the  neck,  one  or  more  inches 
under  the  border  of  the  mandible.  In  some  exceptional  cases  the 
infectious  process  has  spread  under  the  deep  cervical  fascia  to 
discharge  at  some  point  on  the  chest,  and  in  one  case  the  opening 
of  a  sinus  from  a  lower  tooth  was  upon  the  upper  third  of  the 
thigh.  Dentoalveolar  abscesses  in  connection  with  the  lower 
teeth,  more  frequently  than  any  others,  discharge  externally  un- 
der the  mandible,  establishing  submental  fistulae  (Fig.  343). 

In  the  case  of  the  upper  or  lower  teeth,  particularly  if  the  roots 
are  long,  the  buccinator  may  act  as  a  barrier  against  evacuation 
into  the  mouth,  the  infection  in  that  event  spreading  subperios- 
teally  and,  after  causing  a  rupture  of  the  periosteum  at  a  higher 
or  lower  point  beyond  the  attachment  of  the  buccinator  (accord- 
ing as  to  whether  it  is  an  upper  or  a  lower  tooth,  respectively), 
involves  the  overlying  soft  tissues,  causes  an  interstitial  abscess 
among  the  fascial  layers,  and  discharges  at  some  point  on  the  face 
or  jaws.4 

The  symptoms  accompanying  the  involvement  of  the  soft  tis- 
sues of  the  face  or  neck,  in  the  case  of  an  acute  dentoalveolar 
abscess,  which  will  discharge  upon  the  external  aspect,  are  unmis- 
takable.    At  some  area  in  the  swelling  in  the  face  or  neck  the 


4Turner,  J.   G.:      In   "Practice  of  Dental   Surgery,"  by   N.   G.   Bennett. 


430 


DENTAL    PATHOLOGY 


inflammatory  symptoms  are  exaggerated:  there  is  increased  red- 
ness, a  marked  degree  of  heat  to  the  touch,  exquisite  tenderness 
to  palpation,  and  toward  the  last  unmistakable  fluctuation. 
Following  the  rupture  of  the  skin  the  discharge  will  continue 
until  the  cause  is  removed — or  else  will  heal  over  temporarily,  to 
again  discharge  when  exacerbations  of  the  infection  occur  (sub- 
acute abscess.    In  the  event  that  the  cause  is  not  removed,  or  is  only 


Fig.    343. — Submental    sinus.      Opening   of   a   sinus    from   a   subacute   dentoalveolar   abscess 

in  a  lower   incisor. 


partially  so,  the  condition  becomes  chronic.  It  may  be  timely  to 
add  that  a  sinus  leading  from  a  focus  of  infection  to  the  ex- 
terior is  nature's  way  of  eliminating  the  infection  so  far  as  it 
may  be  possible  without  mechanical  or  surgical  interference,  and 
a  more  logical  way  than  that  which  attempts  to  drain  it  through 
the  pinhole  opening  at  the  apex  of  the  root. 

In  some  cases  the  drainage  of  a  dentoalveolar  abscess  takes 
place  through  a  channel  between  the  alveolar  wall  and  its  perios- 


A i  i  Ti:    APICAL    DENTOALVEOLAR    ABSCESS  I'M 

triiin.  and  this  occurs  as  well  in  the  case  of  abscesses  upon  the 
upper  teeth  as  upon  the  lower.  Abscesses  in  connection  with  lower 
molars,  apparently  disobeying  the  laws  of  gravity,  will  discharge 
;it  the  neck  of  the  tooth,  owing  to  the  fact  thai  the  density  of  the 
mandible  in  the  region  of  its  border  offers  a  decided  resistance 
to  the  infectious  process. 

That  stage  of  ;i  dentoalveolar  alisc^s  immediately  preceding  the 
perforation  of  the  alveolar  bone  and  its  periosteum  and  the  in- 
flammatory infiltration  of  the  soft  tissues  is  the  one  accompanied 
by  the  most  severe  pain.  The  piercing  of  the  periosteum  and  the 
invasion  of  the  gum  tissues  and  those  of  the  face  is  marked  by  a 
subsidence  of  the  pain  and  an  increase  in  the  size  of  the  swelling. 
The  invasion  of  the  overlying  soft  tissues  may  give  rise  to  a 
small  and  limited  swelling',  or  to  one  involving  large  areas  of  the 
face  and  neck.  Those  abscesses  in  which  streptococci  are  pres- 
ent in  small  numbers  and  staphylococci  in  large  numbers  cause 
limited  swelling  of  the  soft  tissues,  while  those  in  which  the 
streptococci  are  present  in  large  numbers  give  rise  to  extensive 
involvement  of  the  soft  tissues  of  the  face  and  sometimes  of  the 
neck.  Following  this  stage,  the  inflammatory  discharge  pene- 
trates the  soft  tissues  of  the  gums  and  of  the  mucous  membrane 
lining  the  cheeks  and  spreads  into  the  soft  tissues,  causing  a  cel- 
lulitis, viz.,  a  diffused  or  phlegmonous  involvement  of  soft  tissues. 

Phlegmonous  inflammation  of  the  face,  or  facial  cellulitis  of 
dental  origin  is,  therefore,  the  result  of  the  involvement  by  infec- 
tion of  the  soft  tissues  of  the  face  and  neck,  and  of  the  mucous 
membrane  of  the  mouth  and  marks  the  last  stage  of  an  acute 
dentoalveolar  abscess.  In  some  instances  the  periosteum  is  not 
perforated  at  once,  but  the  pus  remains  under  it  to  find  an  exit 
at  some  point  remote  from  the  seat  of  the  infection.  These  sub- 
periosteal abscesses  or  paridcs,  are  the  ones  usually  causing  acute 
or  chronic  periostitis  and  osteomyelitis  accompanied  by  limited 
or  extensive  necrosis.  The  products  of  the  inflammatory  process, 
by  reason  of  a  strong  resistance  of  the  outer  fibrous  layer  of  the 
periosteum,  do  not  find  a  ready  exit  into  the  overlying  soft  tis- 
sues. The  pus  remains  confined  for  some  time  under  the  perios- 
teum and  the  infectious  process  continues  subperiosteal^  causing 
its  detachment  from  the  bone  and  the  death  of  the  latter  over,  in 


432  DENTAL   PATHOLOGY 

some  cases,  large  areas.  Eventually  it  will  discharge  at  some 
point  distant  from  the  original  focus,  and  in  addition  to  the 
sinus  thus  formed,  other  sinuses  will  lead  from  the  sequestrum 
or  sequestra  to  various  points  on  the  face  or  within  the  mouth. 
In  the  absence  of  early  surgical  intervention  several  sequestra 
will  be  formed  and  the  case  may  assume  alarming  proportions. 


CHAPTER  XXXIII 

PATHOLOGIC  ANATOMY  OF  ACUTE  DENTOALVEOLAR. 

ABSCESS 

A  typical  dentoalveolar  abscess  presupposes  the  death  of  the 
pulp.  The  infection  of  the  peridental  membrane  is  caused  by 
pyogenic  and  other  organisms  previously  engaged  in  the  de- 
struction of  the  pulp  with  suppuration  as  the  result,  and  the  in- 
fection of  the  peridental  membrane  takes  place  by  a  process  of 
continuity.  Once  more  we  are  constrained  to  emphasize  that 
saprophytic  organisms  and  the  by-  and  end-products  of  their 
activity  doubtless  play  some  part  in  the  process  as  previously 
noted.  A  septic  apical  pericementitis,  in  the  sense  that  the  in- 
fection is  at  first  not  at  all  circumscribed,  precedes  the  formation 
of  a  dentoalveolar  abscess. 

One  of  the  first  symptoms  of  pericementitis,  whether  acute 
septic,  or  acute  nonseptic.  is  tenderness  of  the  tooth  to  percussion, 
or  to  any  force,  no  matter  how  slight,  when  applied  against  the 
tooth.  This  symptom  is  due  to  the  congestion  of  the  vessels  of 
the  peridental  membrane,  the  increased  amount  of  blood  having 
reached  that  area  in  response  to  the  increased  stimulus  (the  ir- 
ritant) whether  bacterial,  chemical  or  mechanical.  The  conse- 
quence is  an  undue  pressure  against  the  sensitive  filaments  of  the 
membrane.  The  congestion  of  the  blood  vessels  is  the  hyperemia 
of  the  inflammatory  cycle.  As  the  infection  progresses,  the  tooth 
protrudes  in  its  socket,  consequent  upon  the  presence  among  the 
fibers  of  the  peridental  membrane  of  liquid  and  solid  inflamma- 
tory exudates,  and  of  fibroblasts  of  repair;  this  protrusion  is 
also  the  result  of  the  hydropic  degeneration  of  the  fibers  of  the 
peridental  membrane.  Following  a  momentary  acceleration  of 
the  blood  stream,  in  the  presence  of  an  irritant,  slowing  takes 
place  simultaneously  with  the  rearrangement  of  the  blood  cor- 
puscles— the  red  cells  taking  a  position  in  the  axial  stream,  the 
leucocytes  accumulating  in  the  parietal  stream.  It  is  the  passage 
into  the  meshes  of  the  peridental  membrane  of  a  serous  exudate 
and  multitudes  of  leucocytes,  which  marks  the  beginning  of  the 

433 


434  DENTAL    PATHOLOGY 

subconscious  struggle  on  the  part  of  the  individual  to  successfully 
combat  the  bacteria]  invasion. 

If  the  bacteria  are  in  numbers  or  virulence  unequal  to  the 
power  of  the  body  defenses,  the  symptoms  will  quickly  subside, 
and  there  having  occurred  but  slight  structural  derangement, 
conditions  will  return  to  normal.  Investigations  by  the  author 
have  shown  him  conclusively  that  such  is  the  termination  in  some 
cases  of  mild  infection  of  the  peridental  membrane.  True,  a 
comparatively  small  number  of  cells  may  have  died,  and  some 
may  have  become  the  seat  of  degenerative  changes.  Those  in 
which  the  degenerative  changes  are  slight  may  recover;  those 
in  which  they  are  not,  succumb,  and  these  few,  as  well  as  those 
that  had  at  first  died,  are  carried  away,  probably  in  the  lymph 
of  the  perivascular  lymph  spaces  and  lymph  clefts,  and  by  the 
lymphatics  of  the  cancellated  spaces.  In  the  event  of  an  acute 
dentoalveolar  abscess  developing,  all  the  phenomena  typical  of 
an  acute  inflammation  in  any  other  region  of  the  body  will  fol- 
low in  sequence  with  such  modifications  as  the  topography  of 
the  part  induces. 

The  destructive  infectious  process  affects  first  the  tissues  of  the 
peridental  membrane,  then  those  of  the  surrounding  bony  struc- 
ture, then  those  of  the  overlying  mucous  membrane,  and  finally 
the  products  of  the  septic  inflammation  find  an  outlet  into  the 
mouth;  or  externally  onto  the  face,  as  under  the  mandible  (sub- 
mental fistula  I  ;  or  into  the  maxillary  sinus,  in  the  cases  of  bi- 
cuspids and  molars,  and  of  cuspids,  and  even  of  lateral  incisors. 
Dentoalveolar  abscesses  in  relation  with  the  central  and  lateral  in- 
cisors and  cuspids  may  discharge  into  the  nasal  cavity,  and  in  ex- 
ceptional cases,  especially  following  the  use  of  hot  poultices,  the  in- 
fection may  spread  between  the  deep  cervical  fascia  and  underlying 
muscular  structures  to  discharge  at  some  point  in  the  body  removed 
from  the  head.  In  acute  dentoalveolar  abscess  the  progress  of 
the  infection  is  clinically  observable  in  all  of  its  stages,  and  its 
symptomatology  is  definite  and  unmistakable.  Beginning  with 
the  tenderness  of  the  tooth,  the  redness  of  the  overlying  gum 
tissues,  the  throbbing  character  of  the  pain  increasing  in  in- 
tensity as  long  as  the  inflammatory  exudates  remain  imprisoned 
within  the  unyielding  osseous  tissue  of  the  jaw,  the  decrease  of 
the  pain  concomitantly  with  the  perforation  and  phlegmonous 


PATHOLOGIC    AWTOMV    OF    ACUTE    DENTOALVEOLAB    ABSCESS       435 

involvemenl  of  the  soft  tissues  of  the  mouth  and  face — every 
stage  c;iii  be  easily  identified.  As  the  tissues  of  the  periapical 
peridental  membrane  are  destroyed  following  degeneration, 
death,  ;)n<l  liquefaction  by  the  action  of  the  proteolytic  bacterial 
enzymes,  a  pathway  is  established  into  the  osseous  tissues  of  the 
jaw.  Here  an  acute  osteomyelitis  develops  with  absorption  of 
the  cancellated  bone,  the  process  continuing  through  the  bone 
until  it  reaches  the  periosteum.  In  the  periosteum  an  acute  peri- 
ostitis develops  over  generally  a  small  area,  but  should  there  be 
unusual  resistance  offered  by  the  toughness  and  vascularity  of 
the  periosteum,  the  infection  may  here  assume  a  subacute  or 
chronic  character,  several  days  elapsing  before  a  pathway  is 
established  into  the  soft  tissues  of  the  face.  These  subperiosteal 
abscesses,  or  parules,  are  rarely  of  long  duration,  but  in  the  event 
of  their  becoming  chronic  an  extensive  periostitis  and  osteomye- 
litis ensues,  and  with  them  areas  of  necrosis  in  the  jaw,  upper  or 
lower,  but  more  frequently  in  the  latter.  The  author  recalls  the 
case  of  a  woman,  aged  about  45,  otherwise  in  good  health, 
except  that  extensive  necrosis  developed  in  the  mandible  fol- 
lowing an  acute  exacerbation  of  a  long-standing  infection  in  one 
of  the  roots  of  a  lower  first  molar.  Several  sequestra  were  re- 
moved at  different  times  during  a  period  of  six  months  or  over. 
This  patient  was  in  danger  of  losing  the  greater  portion  of  the 
mandible,  and  only  timely  and  judicious  surgical  and  medicinal 
treatment  prevented  that  serious  ending  of  a  pathologic  condi- 
tion which  at  first  seemed  trivial. 

The  teeth  adjacent  to  the  one  which  is  the  seat  of  an  acute 
dentoalveolar  abscess  may  show  evidences  of  being  involved  in 
the  inflammatory  process.  One  or  two  teeth  on  each  side  may 
become  tender  to  percussion  and  somewhat  mobile  in  their  alveoli 
showing  that  their  respective  peridental  membranes  and  other 
investing  tissues  are  the  seat  of  inflammatory  disturbances.  From 
this,  recovery  is  the  rule  rather  than  the  exception,  upon  sub- 
sidence of  the  acute  infection  in  the  tooth  primarily  responsible 
for  the  infection,  following  suitable  therapeutic  or  surgical  inter- 
ventions. 

The  inflammatory  serous  exudate,  together  with  leucocytes — 
some  dead,  some  in  a  degenerated  condition — and  degenerated 
and  liquefied  fixed  tissue  cells,  are  the  components  of  the  dis- 
charge known  as  pus 


CHAPTEB  XXXIV 

CHRONIC  DENTOALVEOLAR  ABSCESS 

Etiology  and  Pathologic  Anatomy 

By  chronic  dentoalveolar  abscess  is  understood  a  continued  in- 
fection of  low  virulence  located  in  any  portion  of  the  peridental 
membrane.  It  may  he  the  result  of  the  persistence,  in  less  degree, 
of  an  infection  which  had  caused  an  acute  dentoalveolar  abs< — . 
and  again  it  may  exist  unpreceded  by  any  acute  form  of  infec- 
tion. A  chronic  dentoalveolar  abscess  is  in  most  cases  the  result 
of  the  partial  removal  of  the  causes  responsible  for  the  produc- 
tion of  the  acute  form,  through  incomplete  or  defective  technic 
or  inaccessibility  of  root  canals,  or  of  an  extensive  destruction  of 
periapical  fibers  by  an  acute  abscess.  Following  an  acute  dento- 
alveolar abscess,  if  treatment  is  not  at  once  instituted  with  the 
view  t<»  removing  the  infected  contents  of  the  root  canal,  the 
acuteness  of  the  infection  will  in  time  subside,  and  be  followed, 
instead,  by  a  slow  type  of  infection  in  the  periapical  tissues  and 
adjacent  bone  areas.  The  identical  result  will  follow  the  presence 
of  infected  pulp  debris,  through  incomplete  or  defective  technic 
or  inaccessibility  of  root  canals,  or  .from  an  extensive  destruc- 
tion of  periapical  fibers  by  an  acute  abscess.  A  chronic  den- 
toalveolar abscess  may  have  a  sinns  discharging  at  some  point 
in  the  gum  overlying  the  affected  tooth — at  the  gingival  line. 
in  the  maxillary  sinus,  the  floor  of  the  nose,  or  at  some  distant 
point  in  the  mouth  or  face,  or  in  areas  at  a  distance  from  the 
focus  of  infection ;  or  again  it  may  discharge  through  a  root 
canal,  or  it  may  have  no  sinus  whatsoever,  the  latter  being  the 
so-called  "blind  abscess"  of  the  older  nomenclature  to  which 
intly  the  term  "dental  granuloma"  has  been  given.  The 
author  inclines  to  adhere  to  the  old  terminology  of  sinusless 
chronic  dentoalveolar  abscess,  Eor  the  reason  that  pathologically 
it  is  the  reaction  to  the  same  character  of  infection,  in  a  milder 

436 


CHRONIC    DENTOALVEOLAR    A.BS< 


437 


degree  than  that  which  produces  the  acute  form  of  dentoalveolar 
abscess.    The  stronger  infection  is  characterized  mainly  by  tissue 


Fig.   344. — A  chronic  dentoalveolar  abscess   (dental  granuloma)    attached  to   the  root  of 
an  upper  cuspid. 


Fig  343  — Chronic  dentoalveolar  abscess  attached  to  an  upper  incisor  root,  a,  location 
of  apical  portion  of  root;  b,  b,  b,  the  chronic  sinusless  dentoalveolar  abscess  or  so-called 
dental  granuloma. 


destruction;  the  milder,  by  tissue  proliferation  (Figs.  344  and 
345). 


438  DENTAL    PATHOLOGY 

To  the  term  "granuloma"  there  exists  the  objection  that  for 
many  years  prior  to  its  adoption  by  a  group  of  dental  writers, 
general  pathologists  have  given  it  a  definite  place  in  the  study  of 
tissue  reactions  to  specific  chronic  infections.  The  term  granu- 
loma applies,  therefore,  to  certain  tissue  reactions  brought  about 
by  bacteria  and  protozoa  whose  manifestations  are  characteris- 
tically chronic  processes,  to  wit :  Bacillus  tuberculosis,  Bacillus 
lepra?,  Bacillus  mallei,  Spirochete  pallida,  aetinomyces,  blas- 
tomyces,  etc.  In  these  reactions,  in  the  form  of  masses  of  mono- 
nuclear wandering  cells,  surrounded  by  a  wall  of  fibers  and  fibro- 
blasts, there  is  a  breaking  down  when  the  infection  temporarily 
increases  in  virulence,  and  metastases  follow  which  exhibit 
the  same  pathologic  characteristics  as  those  of  the  original  in- 
fection. They  are  modified,  of  course,  by  the  location  and  histo- 
logic characteristics  of  the  tissues  in  which  the  metastatic  mani- 
festation develops,  to  wit.  a  tuberculous  granuloma,  a  syphilitic 
granuloma,  an  actinomycic  granuloma,  etc..  in  each  instance 
metastatic  manifestations  characteristic  of  tuberculosis,  syphilis, 
actinomycosis,  etc.,  being  apparent. 

It  is  not  so.  however,  with  the  tissue  reactions  to  chronic  in- 
fections in  the  apical  peridental  membrane.  These  sinusless 
chronic  dentoalveolar  abscesses — so-called  blind  abscesses,  in  the 
sense  that  they  have  no  external  avenue  of  drainage — when  in 
the  course  of  exacerbations  of  the  infection,  and  following  a  de- 
crease in  the  vital  resistance  of  any  portion  of  the  body,  may 
bring  about  one  of  any  number  of  pathologic  conditions,  e.g.. 
arthritis,  gastric  or  intestinal  ulcers,  nephritis,  endocarditis,  peri- 
carditis, myocarditis,  pernicious  anemia,  disorders  of  metabolism, 
neuralgia,  neuritis,  etc.  AVe  shall  adhere  to  the  older  nomencla- 
ture, and  in  describing  the  etiology,  pathology,  and  symptoms,  the 
student  should  bear  in  mind  that  the  terms  "sinusless  chronic 
dentoalveolar  abscess."  or  "blind  abscess,"  or  "dental  granu- 
loma," are  used  interchangeably. 

To  recapitulate,  let  us  say,  therefore,  that  a  chronic  dento- 
alveolar abscess  may  assume  any  one  of  the  following  forms: 

1.  A  chronic  dentoalveolar  abscess  with  a  sinus. 

2.  A  chronic  dentoalveolar  abscess  without  a  sinus — the  so- 
called  "blind  abscess"  of  the  old  nomenclature,  or  dental  granu- 
loma. 


CHRONIC    l'l  vi'n  \i.\  EOLAE     i.BS<  I  SS  430 

:;.  a  chronic  dentoalveolar  abscess  discharging  through  a  rool 
canal. 

4.  A  chronic  dentoalveolar  abscess  with  ;i  sinus  along  the  side 
of  the  runt,  discharging  a1   the  gingival  margin. 

In  the  case  of  an  acute  dentoalveolar  abscess  the  shorl  time  in 
which  tin-  infection  remains  in  the  periapical  lissues  is  probably 
the  reason  extensive  detachments  of  peridental  fibers,  with  conse- 
quenl  areas  of  cementum  necrosis,  occur  rarely.  The  reverse  of 
this  obtains  in  the  chronic  form  in  which  the  infection  in  the 
periapical  tissues  is  kept  up  from  the  root  canals,  causing  rela- 
tively extensive  detachment  and  destruction  of  peridental  fibers, 
and  areas  of  cementum  necrosis,  following  exacerbations  of  the 
infection  and  the  overcoming  of  the  inflammatory  elements  by 
the  reactivated  bacteria.  These  areas  of  cementum  necrosis  oc- 
cur in  the  sinuslos  chronic  dentoalveolar  abscess,  and  also  in  those 
which  discharge  through  a  sinus  or  root  canal. 

There  is  usually  no  pain  connected  with  a  sinusless  chronic 
dentoalveolar  abscess,  although  a  sense  of  heaviness  in  the  affected 
tooth  or  neighboring  teeth  may  lie  experienced.  Some  of  the  worst 
eases  of  systemic  involvement  under  the  author's  observation  from 
sinusless  chronic  dentoalveolar  abscess  developed  even  in  cases 
in  which  the  chronic  abscesses  gave  rise  to  no  symptoms  whatso- 
ever, either  objective  or  subjective. 

Early  in  the  course  of  our  studies,  before  the  x-ray  was  avail- 
able as  a  routine  adjunct  in  dental  practice,  our  attention  was 
centered  on  a  form  of  a  chronic  pericemental  inflammation  in- 
duced by  a  bacterium  apparently  of  a  degree  of  virulence  giving 
rise  to  ehronicity  of  symptoms.  The  patients  would  invariably 
relate  a  history  of  pulp  necrosis,  or  of  intentional  pulp  devitaliza- 
tion with  subsequent  treatment  and  filling  by  generally  approved 
methods  of  practice,  and  very  frequently  they  reported  to  have 
experienced  no  degree  of  discomfort  since  then.  Upon  examina- 
tion, both  visual  and  percussive,  no  definite  indication  could  be 
obtained  as  to  the  conditions  existing  in  the  periapical  tissues; 
but  by  locating  the  upper  third  of  the  tooth  root  and  exerting 
pressure  with  the  finger  near  the  apex,  a  certain  degree  of  tender- 
ness would  be  elicited  in  some  cases. 

A  number  of  cases,  upon  being  reopened  under  aseptic  pre- 
cautions and  upon   being  subjected  to   appropriate   medication, 


440  DENTAL   PATHOLOGY 

would  remain  in  status  quo;  i.  e.,  conditions  would  still  be  as  they 
were  at  the  time  the  suggestion  to  retreat  them  was  made. 
Neither  pain  nor  any  degree  of  discomfort  appreciable  by  the 
patient  had  been  the  warrant  for  the  additional  treatment  which 
in  our  opinion  seemed  to  be  indicated.  These  eases  were  given 
further  consideration  with  the  purpose  in  view  of  ascertaining, 
if  possible,  what  bearing  they  could  have  upon  the  patient's  evi- 
dent decrease  in  physiologic  power — an  interruption  in  the  nor- 
mal balance  of  assimilation,  dissimilation  and  elimination — and 
upon  the  presence  of  pain  in  various  regions  of  the  body,  of  ob- 
scure origin.  The  subjective  symptoms  would  include  such  head- 
ings as  headaches,  lassitude,  migraine,  indigestion,  nephritis,  mel- 
ancholia, arthritis,  reflex  pain,  loss  in  body  weight,  decreased 
appetite,  etc.  In  some  of  these  cases,  hesitating  at  first  to  assume 
an  ultraradical  form  of  intervention.  Ave  endeavored  to  eliminate 
the  infection  from  the  root  canals  and  to  refill  them  completely, 
but  even  then  the  results  were  still  unsatisfactory  as  the  systemic 
symptoms  continued  unabated.  In  other  cases  in  the  same  class, 
and  as  years  went  on.  we  assumed  the  positive  attitude  that  in 
the  event  of  failure  to  restore  the  teeth  to  their  normal  condition 
by  the  methods  of  therapeutics  at  our  command,  their  removal 
would  be  effected.  Needless  to  add,  many  cases  were  there- 
fore sacrificed  to  the  extracting  forces,  but  in  so  doing  the  sys- 
temic welfare  of  the  patient  was  being  continuously  borne  in 
mind,  and  not  the  efficiency  of  his  masticatory  apparatus.  And 
we  may  add  that  in  most  cases  an  abeyance  of  the  general  symp- 
toms resulted,  in  many  cases  so  treated  complete  recovery  even- 
tually folloAving.  , 

Looseness  of  a  tooth  which  is  the  seat  of  a  chronic  dentoalveolar 
abscess  is  not  invariably  present,  and  in  order  that  it  should  be 
marked  it  is,  of  course,  necessary  that  a  decided  area  of  detach- 
ment should  have  occurred  in  the  apical  region  of  the  root.  In  cases 
of  this  kind  looseness  will  be  perceptible ;  otherwise  a  tooth  may 
be  the  seat  of  a  chronic  dentoalveolar  abscess  and  still  be  firm 
in  its  socket. 

Percussion  as  a  reliable  means  of  diagnosing  inflammations 
of  the  peridental  membrane,  either  acute  or  chronic,  may  be 
advantageously  discussed  at  this  time.  It  is  to  be  regretted 
that   the  majority   of  dental   practitioners   do   not   avail   them- 


CHRONIC    DENTOALV1  OL  \i:    ABSi  I  I  1 

selves  of  this  method  of  ascertaining  the  degree  of  involve- 
iiinii  of  the  peridental  membrane  and  alveolar  hone.  The 
tone  produced  by  percussing  a  tooth  with  the  handle  of  a  metal- 
lic instrument  is  sharp  and  acute  when  the  peridental  membrane 
is  healthy.  1  i'  the  peridental  membrane  is  at  all  diseased  the 
sharpness  of  the  tone  is  absent,  and  instead  a  dull  note  is  pro- 
duced. \\\  percussing  a  tooth,  for  instance  a  central  incisor,  ii 
should  be  percussed  on  the  lingual  surface,  on  the  laltial  surface 
and  on  the  incisal  edge,  a  molar  should  be  percussed  on  the 
buccal  or  lingual  surface,  and  each  cusp  should  be  percussed  sep- 
arately. If  the  index  finger  of  the  left  hand  be  placed  upon  the 
gum  overlying  the  root  or  roots  of  the  tooth  percussed,  the  greater 
the  area  of  rarefaction,  if  toward  the  labial  or  buccal  side,  the 
greater  will  be  the  perception  of  vibrations  by  the  operator's 
finger.  Lately  Talbot  has  discussed  percussion  as  a  means  of 
diagnosis,  and  with  his  conclusions  we  are  in  entire  harmony, 
having'  practiced  percussion  in  the  diagnosis  of  pericemental  dis- 
ease for  many  years. 

In  the  course  of  pulp  suppuration  and  putrefaction,  or  both, 

which  is  the  precursor  of  apical  pericemental  infection,  the  tooth 
may  become  discolored  in  the  majority  of  cases.  The  discolora- 
tion varies  in  intensity,  beginning  with  a  slightly  pink  hue.  which 
develops  in  the  stage  of  pulpitis,  and  increasing  through  the  reds, 
browns,  and  blacks  of  advanced  decomposition  of  hemoglobin,  and 
thence  to  the  grays,  greens  and  blacks,  the  result  of  chemical 
reactions  consequent  upon  pulp  putrefaction.  It  therefore  hap- 
pens that  teeth  which  are  the  seat  of  chronic  or  of  acute  dento- 
alveolar  abscesses  exhibit  frequently  some  degree  of  discolora- 
tion. All  pulpless  teeth,  even  when  no  discoloration  lias  ensued, 
do  not  possess  the  same  degree  of  transluceney  as  is  the  case 
in  teeth  with  live  pulps. 

A  chronic  infection  of  the  peridental  membrane,  it  should  be 
here  noted,  may  have  for  its  reaction  not  only  a  chronic  dento- 
alveolar  abscess,  but  instead  in  some  instances,  although  rela- 
tively few,  cysts  may  develop:  and  in  these  cysts  not  infrequently 
is  to  be  found  evidence  of  the  proliferation  of  epithelial  rem- 
nants of  the  peridental  membrane.  Instances  of  dentigerous  or 
root  cysts  which  developed  in  connection  with  roots  which  had 
been  the  seat  of  mild  chronic  inflammations  are  shown  at  Figs. 


44:i 


DENTAL   PATHOLOG? 


346,  347,  :<4^.  and  349.  These,  together  with  their  complete  his- 
tories, were  furnished  me  by  Dr.  E.  F.  Tholen,  Los  Angeles,  and 
some  are  on  record  in  the  periodical  literature.*  These  epithelial 
remnants  which  were  originally  observed  by  Black,  and  by  him 
called  a1  first  the  glands  of  the  peridental  membrane,  have  since  been 


Fig.  346. — Dentigerous  or  root  cyst  as- 
sociated in  its  etiology  with  a  sinusless 
chronic  dentoalveolar  abscess  in  an  upper 
first  bicuspid. 


Fig.      .?47. — Dentigerous     or     root     cyst 

which  extended  to  the  molar  region  on  the 
right  side  associated  in  its  etiology  with 
an  injury  in  the  upper  right  lateral  fol- 
lowed by  a  chronic  dentoalveolar  abscess. 
The  existence  of  the  cyst  was  ascertained 
nine   years   after   the   injury   was   sustained. 


Fig.    348. — Dentigerous   or   root   cyst   as-  Fig.     349.— Dentigerous     or     root     cysts 

ted     in     its     etioiogy     with     a     chronic  associated  in  etiology  with  a  chronic  dento- 

dentoalveolar  abscess  in  an  upper  second  alveolar  abscess  in  an  upper  first  bicuspid. 
bicuspid. 

shown  to  he  the  remnants  of  the  enamel  organ — the  epithelial 
cells  of  which  have  become  entangled  in  the  peridental  tissues 
wherein  they  remain  quiescent  until  a  certain  degree  of  irrita- 
tion leads  To  their  proliferation.  Black  admitted  at  no  time  that 
these   epithelial   elements   were   remnants   of  the   enamel   organ, 


'Pacific    Dental    Gazette,    xxv,    p.    781. 


CHRONIC    DENTOALVEOLAR    ABSCESS  443 

stating  that  he  had  followed  the  breaking  up  of  the  cells  of  the 
enamel  organ.  "1  have  seen  them  float  away,"  he  says,  "with 
the  tissues  in  groups,  forming  epithelial  pearls,  some  large  and 

some  very  small.  I  have  followed  them  from  one  age  of  an  ani- 
mal to  another  ago,  and  as  I  have  thus  followed  them,  I  have 
found  that  they  were  absorbed  and  disappeared  completely." 
The  question  remains  as  yet  unsolved,  although  the  evidence  is 
strongly  in  favor  of  the  opinion  which  considers  these  epithelial 
groupings  as  derived  from  the  enamel  organ. 

Mild  chronic  inflammation  of  the  peridental  membrane  brings 
about  thickenings  of  the  membrane,  circumscribed  or  diffused. 
These  thickenings  represent  round-cell  infiltration,  hydropic  de- 
feneration and  proliferation  of  fixed  fibers  of  the  peridental 
membrane. 

Difference  in  the  Pathology  of  Acute  and  Chronic  Dentoalveolar 

Abscess 

The  difference  in  pathology  between  acute  and  chronic  dento- 
alveolar abscesses  is  just  the  difference  in  reaction  between  an  in- 
fection leading  at  once  to  tissue  destruction  with  little  prolifera- 
tion of  fibroblasts;  and  one  which,  because  of  low  bacterial  vir- 
ulence, over  a  prolonged  period  of  time,  brings  about  an  initial 
detachment  of  the  fixed  fibers  of  the  peridental  membrane  on 
the  alveolar  side  with  a  subsequent  walling  off  of  the  infected  area 
by  fibers  which  are  the  proliferations  of  the  fixed  fibers  of  the 
peridental  membrane,  this  structure  enclosing  large  masses  of 
mononuclear  wandering  cells. 

Why  the  chronic  reaction  should  be  termed  a  granuloma  is  be- 
yond justification.  Neither  is  it  a  tumor  in  the  sense  of  a  neo- 
plasm, nor  is  granulation  tissue  the  characteristic  of  its  contents. 
It  is  purely  the  reaction  to  bacteria  of  less  numbers  and  of  lower 
virulence  (actual  or  relative)  than  is  the  ease  with  the  acute 
form  of  dentoalveolar  abscess.  True  that  fibroblasts  of  repair 
may  be  seen  within  the  circumscribed  mass  of  leucocytes  and  bac- 
teria ;  but  they  are  present  in  small  numbers,  and  as  long  as  the 
infection  persists  they  play  a  decidedly  insignificant  role.  The 
essential  characteristics  are  the  fibrous  envelope  and  the  mono- 
nuclear wandering  cells  contained  therein  (Figs.  350-355).  These 
cells  may   be  lymphocytes,   small   and  large,  mononuclear  leuco- 


444 


DENTAL    PATHOLOGY 


cytes,  small  and  large,  and  plasma  cells  in  decidedly  less  numbers 
than  any  of  the  other  forms.  Some  polymorphonuclear  leucocytes 
are  also  present.  Recently  Hartzell,  in  an  exhaustive  study  of  the 
microscopic  anatomy  of  chronic  dentoalveolar  abscess  (dental 
granuloma),3  asserts  that  the  majority  of  these  mononuclear 
wandering  cells  are  plasma  cells.  In  order  to  have  a  clear  under- 
standing of  the  cellular  constituents  of  a  sinusless  chronic  dento- 
alveolar abscess,  sections  should  be  studied  microscopically  under 


6- 


b— 


b— 


Fig.    .350. — Chronic    dentoalveolar    abscess    (so-called    dental    granuloma),      a,   abscess    sac 
b,   b,   b,   round-cell   infiltration   which   constitutes   the   bulk  "I"  the  abs 


a  high  power  (Fig.  356).  A  detailed  reference  to  the  forms  of 
leucocytes  that  are  to  be  found  within  the  circumscribed  mass 
will  doubtless  aid  the  student  in  the  task  of  cell  identification  in 
a  sinusless  dentoalveolar  abscess  (dental  granuloma). 

The  polymorphonuclear  neutrophile  leucocytes  constitute  nor- 
mally about  65  to  70  per  cent  of  the  circulating  leucocytes  in  the 
adult,  and  from  18  to  40  per  cent  in  the  child.  These  cells  are 
from  10  to  12  microns  in  diameter.  They  are  derived  from  the 
neutrophile  myelocytes  which  arc  found  in  bone  marrow  and 
which     are     the     descendants     of     the     mononuclear     myeloblast 


'Journal   of   the   National    Dental   Association. 


CHRONIC    DENTOALVEOLAB    ABS( 


445 


with  neutrophile  or  occasionally  eosinophile  granules— a  cell  sev- 
eral   times    Larger    than    the    polymorphonuclear    Leucocyte.      The 


b— 


Fig.    351. — Section    of    a    chronic    dentoalveolar    abscess    (dental    granuloma)     showing 
a   portion   of  the   fibrous   wall   and   of  the   body   of   the   al  anuloma).      The    i 

wall  present-  areas  of  round-cell  infiltration  similar  in  their  composition  to  the  mass  which 
makes  up  the  bod)  of  the  abscess.  The  fibrous  wall  is  not  an  absolute  harrier  to  the  in- 
fection, a,  fibrous  wall;  h,  round-cell  infiltration  making  up  the  hulk  of  the  abscess  (only 
a  small  area  is  shown):    c,   areas   of  round-cell   infiltration   in   the   fibrous   wall. 


nucleus  in  the  polymorphonuclear  neutrophile  leucocyte  assumes 
any  one  of  a   number  of  irregular  shapes:  it   may  be  U-shaped 


446 


DENTAL   PATHOLOGY 


with  nodular  enlargements,  or  S-shaped  and  likewise  with  nodu- 
lar enlargements;  or  it  may  be  composed  of  several  separate  nu- 


Fig.    352. — Chronic    dentoalveolar    abscess.      High    power   photomicrograph    of   a   portion    of 
the   fibrous  wall,     a,  a,   fibrous  wall. 

clear  bodies.  The  nucleus  has  an  abundance  of  chromatin  fibers. 
These  cells  are  strong  phagocytes  for  bacteria.  When  found  in 
pyogenic  discharges  these  are  the  so-called  pus  cells.     A  some- 


CHRONIC    DENTOALVEOLAH    ABSCESS 


447 


whal  similar  polymorphonuclear  form  with  granular  protoplasm 
having  a  strong  affinity  for  eosin,  known  as  the  polymorphonu- 
clear eosinophile,  exists  in  small  proportions  Prom  1  to  2  per  cent. 
They  are  derivatives  of  the  mononuclear  eosinophilic  myelocyte 
of  bone  marrow.  These  polymorphonuclear  eosinophiles  have 
Larger  nuclei  with  coarser  fibers  than  those  of  the  neutrophilic 
forms.  They  have  less  phagocytic  power  than  the  neutrophile, 
hnt   nevertheless  appear  early  in  some  acute  inflammations. 


Fig.  353. — Chronic  dentoalveolar  abscess  (dental  granuloma).  Oblique  decalcified 
section.  The  origin  of  the  libers  which  form  the  fibrous  wall  is  from  proliferations  from 
the  preexisting  fillers  of  the  peridental  membrane,  a,  a,  dentin;  h.b,  cementum;  c,  c, 
libers  of  the  peridental  membrane;  d.d.  beginning  of  the  fibrous  wall;  c,c,  proliferations 
from   the   preexisting   fibers   of   the   peridental    membrane. 


The  lymphocytes  which,  according  to  their  size,  are  known  as 
small  and  large,  constitute  approximately  20  per  cent  of  the  total 
number  of  leucocytes  in  the  normal  adult  blood,  and  from  40  to  60 
per  cent  in  the  infant.  The  small  are  from  5  to  8  microns  in  diame- 
ter, the  large  from  8  to  10  microns.  Their  protoplasm  is  strongly 
basic,  showing  as  a  blue,  narrow  margin  surrounding  a  clear  or 


448 


DENTAL    PATHOLOGY 


pale  nucleus  which  lakes  up  most  of  the  cell  and  which  is  round, 
or  nearly  so.  The  large  and  small  lymphocytes  are  probably  one 
and  the  same  cell,  the  larger  probably  being  the  older.  The 
lymphocytes,  as  well  as  the  mononuclear  Leucocytes  yet  to  be  de- 
scribed, play  an  unimportant  part  in  chronic  inflammations,  but 
not  so  in  the  acute.  They  are  not  phagocytic  for  bacteria,  but 
are  so  for  portions  of  cells  in  process  of  disintegration  and  foreign 
matter  other  than  bacteria. 


marked    contrast    between    Imlk    of    ab- 


Fig     354. — Chronic    dentoalveolar    abscess    showing 

and   fibrous   wall,     a,  a,  bulk   of  absciss;    b,  b,    fibrous   wall. 


The  large  and  small  mononuclear  leucocytes  are  present  in 
from  3  to  5  per  cent.  The  large  ones  are  from  12  to  15  microns. 
therefore  Larger  than  even  the  large  lymphocyte.  The  small  ones 
are  differentiated  from  lymphocytes  by  the  nucleus  being  ec- 
centrically located  and  not  clearly  outlined,  and  surrounded  by  a 
relatively  large  amount  of  protoplasm,  as  compared  with  the 
lymphocyte.  The  protoplasm,  which  is  free  from  granules,  is  less 
basophilic  than  the  nucleus. 


CHRONIC    DENTOALVEOLAB    ABS< 


440 


McCallum   is  of  the  opinion  that   all   mononuclear  wandering 
cells  originate  from  one  of  three  sources  : 

d  d 


/___. 


Ckl b 


L 


p;„     3^5 Chronic    dentoalveola  died    dental    granuloma).      Longitudinal 

decalcified  section  A  large  number  of  fibers  are  seen  which  have  proliferated  from  the 
fixed  cells  of  the  peridental  membrane.  The  libers  at  a,  a,  constitute  part  of  the  fibrous 
sac  Groups  of  libers  are  seen  at  b,  b.  which  penetrate  into  the  chronic  dentoalveolar 
abscess  for  a  short  distance.  The  libers  of  the  peridental  membrane  at  c.c.c.  do  not 
appear  to  have  been  destroyed  but  merely  to  have  proliferated;  d.  d,  cementum;  e,  c. 
dentin;  f.f.f.  areas  of  round-cell  infiltration.  The  bulk  of  the  abscess  would  be  beyond 
the   right   of   the   picture. 


450 


DENTAL    PATH' 


1.  The  reticulum  cells  and  the  endothelial  cells  of  the  sinuses  in 
lymph  nodes,  the  lymph  nodes  of  the  intestine  and  in  the  spleen. 

2.  From  cells  which  are  normally  found  in  the  adventitial  tis- 

a       b 


d 


Fig.  350. — High  power  reproduction  of  cellular  elements  in  the  round-cell  infiltration 
in  a  chronic  dentoalveolar  abscess  (dental  granuloma).  Mononuclear  wandering  cells 
predominate,  viz.,  mononuclear  leucocytes,  lymphocytes  and  plasma  cells ;  fibroblasts  are 
also  to  be  seen,  a,  a,  plasma  cells;  b,  b,  b,  lymphocytes,  c,  c,  mononuclear  leuco 
d,  group  of  mononuclear  leucocytes;  e,  large  mononuclear  leucocyte;  /,  polymorpho- 
nuclear neutrophile  leucocyte;  g,  g,  fibroblasts. 


CHRONIC    DENTOALVEOLAR    ABSCESS  151 

sues  of  vessels,  and  scattered  elsewhere  in  the  crevices  of  tissues. 

3.  From  lymphocytes  which  emigrate  from  the  blood  vessels, 
and  in  the  tissues  developed  into  ameboid  forms,  quite  like  those 
already  there. 

The  origin  of  the  mononuclear  forms  is  attributed  by  Mallory 
to  the  endothelial  cells  of  capillaries.  The  doubl  which  exists  as 
to  their  source  should  not  mislead  the  student  into  considering 
the  wandering  cells  of  any  kind  as  of  subsidiary  diagnostic  im- 
portance. Such  is  by  no  means  the  case,  as  the  determination  of 
the  several  classes  of  leucocytes  is  essential  in  the  study  and 
diagnosis  of  inflammatory  conditions  in  general,  including  those 
which  develop  in  the  pulp  and  investing  tissues. 

The  plasma  cell  of  Unna,  a  mononuclear  wandering  cell,  is 
probably  derived  from  the  lymphocyte.  It  occurs  normally  in 
mucous  membranes  and  is  present  in  large  numbers  in  chronic 
and  subacute  inflammation.  Certain  peculiarities  of  the  plasma 
cell  are  constant.  The  nucleus  is  surrounded  by  a  halo  or  vacuole, 
and  is  located  eccentrically.  The  nucleus  has  a  coarse  appearance 
and  the  protoplasm  takes  a  bluish  stain  with  ordinary  nuclear 
dyes.2 

A  chronic  dentoalveolar  abscess  is.  as  previously  stated,  the 
reaction  to  a  protracted  infection  of  low  virulence,  and  is  consti- 
tuted of  a  mass  of  inflammatory  cells  surrounded  by  a  fibrous 
wall,  composed  of  cells  which  have  proliferated  from  the  preex- 
isting fibers  of  the  peridental  membrane.  The  envelope  of  the 
abscess  is  a  strong  fibrous  capsule  or  sac,  within  which  are  to  be 
found  the  inflammatory  elements  and  some  fibroblasts;  in  addi- 
tion, blood  vessels  are  to  be  found  immediately  adjacent  to  and 
within  the  fibrous  cell.  The  bulk  of  the  dentoalveolar  ahseess  is 
made  up  of  mononuclear  leucocytes  in  large  numbers,  polymor- 
phonuclear leucocytes  in  restricted  numbers,  plasma  cells,  and  a 
few  fibroblasts.  The  capsule  does  not  necessarily  mark  the  bound 
ary  of  the  abscess,  for  beyond  the  capsule  the  author  has  found  a 
continuity  of  it. 

Trabeculated  abscesses  are  not  uncommon,  two  or  more  com- 
partments entering  into  the  formation  of  one  single  chronic 
dentoalveolar  abscess  (dental  granuloma'). 

-McCallum,    W.    G.:      A    Textbook   of    Pathology,    Wm.    Wood    &    Co. 


452  DENTAL    PATHOLOGY 

Bacteria  of  Septic  Pericementitis  and  Dentoalveolar  Abscess 

The  organisms  concerned  in  the  process  of  suppurative  inflam- 
mation of  the  periapical  tissues  are  practically  the  same  organ- 
isms as  are  responsible  for  the  development  of  suppuration  in 
other  regions  of  the  body.  These  organisms  are  various  strains 
of  streptococci,  tht  Staphylococcus  pyogenes  albus,  aureus,  and 
citreus;  and  occasionally  the  diplococcus  of  pneumonia.  In  a 
series  of  bacteriologic  investigations  by  Schreier,  the  diplococcus 
of  pneumonia  was  found  in  large  numbers  in  a  series  of  fifteen 
cases  out  of  a  total  of  twenty.  In  these  infections  has  also  been 
found  the  organism  isolated  by  Arkovy  from  gangrenous  pulps, 
which  he  named  the  Bacillus  gangrena  pidpce. 

In  gangrenous  as  well  as  in  suppurating  pulps,  Miller1  found 
in  addition  to  the  foregoing  organisms  the  Bacillus  pulp"  pyo- 
genes, an  organism  which  occurs  either  singly  or  in  pairs,  or  in 
chains  of  four  to  eight.  It  produces  liquefaction  of  gelatin  in 
eighteen  to  twenty  four  hours  from  the  time  of  inoculation.  The 
same  investigator  reports  finding  in  a  suppurating  pulp  a  thick, 
short  bacterium  with  rounded  ends,  one  and  a  half  to  four  times 
as  long  as  thick.  This  organism,  designated  by  him  as  the  Bac- 
terium gingiva  pyogenes,  liquefies  gelatin,  and  when  injected  into 
the  abdominal  cavity  of  white  mice  produced  death  in  ten  to 
twenty-five  hours. 

Recently  Gilmer  and  .Moody1  have  obtained  from  alveolar  ab- 
scess and  infected  root  canals,  three  strains  of  streptococci.  A 
hemolytic  streptococcus,  producing  a  wide  zone  of  hemolysis 
was  found  in  the  acute  form  and  the  Streptococcus  viridans  and 
a  Streptococcus  mucosas  was  found  in  the  chronic  forms.  These 
three  strains,  particularly  the  Streptococcus  viridans,  grow  both 
anaerobically  and  aerobieally.  The  anaerobic  cultures  which 
contain  streptococci,  these  investigators  found,  are  rarely  pure. 
The  streptococcus  is  rarely  found  alone,  it  having  been  present 
in  the  infections  studied  by  these  investigators  in  association 
with  B.  fusiformis.  When  cultured  aerobieally  only  occasionally 
did  they  find  the  staphylococcus  albus  or  aureus,  the  micrococcus 
catarrhalis,  and  some  unidentified  saprophytic  organism.     In  two 


'Miller,  W.   I).:      -Microorganisms  of  the  Human  Mouth. 

'A   Study  of  the  Bacteriology  of  Alveolar  Abscess  and  Infected   Root  Canals,  Jour.  Am. 
M.  d.   Assn. 


CHRONIC    DENTOALVEOLAR    ABSCESS  !•">•"> 

instances  they  found  diphtheroid  bacillus  which  grew  both  an- 
aerobically  and  aerobically. 

Additional  facts  of  interest  concerning  the  bacteriology  of  al- 
veolar abscess  and  infected  rool  canals  are  quoted  from  Gilmer 
and   Moody  *s  reporl  : 

"Anaerobically,  in  old  cultures,  we  have  seen  in  material  from 
three  different  abscesses  a  black-pigment-producing  organism. 
This  organism  is  slow-growing  and  does  not  usually  appear  for 
about  five  days.  We  do  not  believe  that  it  is  of  any  importance 
in  these  infections. 

"In  three  of  1  lie  chronic  eases  from  which  material  was  ex- 
amined the  patients  were  treated  with  autogenous  vaccines  with 
striking  beneficial  results.  The  vaccines  were  made  from  the  cul- 
tures of  both  the  aerobic  and  anaerobic  organisms,  and  were 
given  in  graded  doses  at   five-day  intervals. 

"These  were  chronic  suppurations,  following  that  class  of  acute 
infections  of  the  mandible  characterized  by  much  brawny  swell- 
ing, persisting  over  a  week  or  more  with  little  or  no  indications 
of  pointing.  The  pus  discharge  continued  with  no  seeming 
diminution  for  several  weeks  after  the  acute  symptoms  had  sub- 
sided. In  each  instance  the  pus  flow  stopped  promptly  on  the  use 
of  the  vaccine  treatment. 

"Those  who  have  made  extensive  observations  of  the  tendency 
of  acute  attacks  of  alveolar  abscess  recognize  that  they  occur 
epidemically.  Whether  the  epidemics  of  streptococcus  nose  and 
throat  infections  follow  or  occur  simultaneously  with  epidemics  of 
alveolar  abscess  is  a  question  both  of  interest  and  importance. 
We  have  not  sufficient  data  to  warrant  a  definite  statement  rela- 
tive to  the  subject,  however,  since  we  have  found  in  both  infec- 
tions the  same  bacteria,  and  as  both  occur  epidemically,  it  may  be 
discovered  that  there  is  a  \ery  definite  relationship  between  the 
two  infections. 

"It  seems  reasonable  to  suppose  that  the  presence  of  the  strep- 
tococcus of  nose  and  throat  infections  may  easily  cause  simul- 
taneous or  secondary  infections  in  the  jaws,  the  organisms  reach- 
ing the  apices  of  the  roots  through  cavities  of  decay  in  the  teeth, 
or  through  the  circulatory  channels." 

Eos  enow"'  has  made  cultures  from   the   pus  withdrawn  from  a 


5Rosenow,   E.   C. :      The   Pathogenesis   of  Focal  Infection,   Jour.   National   Dental   Assn. 


454  DENTAL   PATHOLOGY 

chronic  dentoalveolar  abscess  with  sinus  and  has  obtained  al- 
most pure  culture  of  Streptococci  viridans  in  association  with  a 
few  colonies  of  Streptococcus  hemolyticus.  He  has  also  obtained 
from  a  chronic  dentoalveolar  abscess  a  short  chained  streptococ- 
cus. The  cultures  from  the  pulp  of  the  same  tooth  after  extrac- 
tion yielded  two  days  later  the  same  organisms  that  were  isolated 
from  the  pus  of  the  abscess. 


CHAPTER  XXXV 

BONE 

Normal  and  Pathologic  Considerations 

Bone  is  a  form  of  connective  tissue  impregnated  with  lime 
salts.  There  are  two  varieties  of  bone,  spongy  or  cancellated,  and 
compact.  The  spongy  bone  is  the  fundamental  form,  yet  only  in 
the  compact  form  are  all  the  structural  peculiarities  of  bone 
present.  A  cross  section  of  compact  bone  shows  a  number  of 
round  openings,  the  Haversian  canals.  The  central  opening  of  a 
Haversian  canal  is  surrounded  by  layers  of  bone  concentrically 
arranged — the  concentrically  disposed  lamellce — this  canal  and 
the  surrounding  lamellae  forming  a  Haversian  system.  In  the 
longitudinal  section  the  course  of  these  canals  seems  to  corre- 
spond to  the  long  axis  of  the  bone,  although  some  run  obliquely 
and  establish  communication  between  adjacent  canals.  All  the 
Haversian  canals  communicate  with  the  central  marrow  cavity 
and  may  be  viewed  in  the  light  of  continuations  from  it.  Each 
Haversian  canal  contains  bone  marrow — myelitic  substance — a 
tissue  richly  supplied  with  blood  vessels,  lymphatics  and  nerves. 
The  spaces  between  the  Haversian  systems  are  filled  by  short 
lamellae,  which  are  not  arranged  in  any  definite  way — the  inter- 
stitial or  ground  lamellce.  The  circumferential  lamellae  are  those 
which  surround  the  bone  on  its  outer  and  inner  circumference; 
i.e.,  they  are  located  immediately  under  the  periosteum  and 
around  the  central  marrow  cavity.  In  the  ground  matrix  are 
located  the  lacuna-,  from  which  minute  channels  radiate — the 
canaliculi.  Each  lacuna  contains  connective  tissue  elements,  the 
bone  corpuscles.  These  bone  cells  exhibit  processes  which  ex- 
tend into  the  canaliculi.  The  lacunas  of  a  Haversian  system  com- 
municate with  one  another  by  means  of  their  canaliculi,  but  not 
with  the  canaliculi  of  adjoining  systems.  The  channels  through 
the  circumferential  lamellae  which  carry  blood  vessels,  lymphatic 
vessels,  and  nerves  from  the  periosteum  to  the  Haversian  canals, 
and  those  which  run  across  the  inner  circumferential  lamellae  to 
the  central  marrow  cavity,  are  known  as  Volkmann's  canals. 

455 


456  DENTAL    PATHOLOGY 

Bone  is  surrounded  by  a  nitrous  membrane,  the  periosteum.  It 
consists  of  two  layers — the  outer  fibrous,  dense  protective  layer; 
and  an  inner,  less  dense  layer  very  rich  in  blood  vessels  and  com- 
posed of  delicate  white  and  elastic  fibers.  The  inner  layer  is  con- 
cerned with  the  formation  of  bone  and  is  known  as  the  osteoge- 
netic  layer.  The  outer  layer  contains  the  larger  blood  vessels,  the 
inner  layer  the  smaller  though  more  numerous  blood  vessels.  The 
osteoblasts  are  located  in  the  osteogenetic  layer.  The  fibers  of 
Sharpey  are  fibers  from  the  periosteum  which  have  remained  in 
the  lamellae  without  undergoing  calcification.  The  central  cavity 
and  all  cancellated  spaces  are  filled  with  marrow  of  which  two  va- 
rieties are  recognized,  the  red  and  the  yellow,  the  red  being  the 
younger  variety  and  the  yellow  the  older.  Bone  marrow  is  a 
bb.od-forming  organ  and  consequently  contains  all  varieties  of 
blood  cells  as  well  as  myelocytes,  nucleated  red  blood  cells,  giant 
cells,  fat  cells,  mast  cells,  etc.  Bone  marrow  consists  of  a  delicate 
connective-tissue  framework  supporting  a  rich  supply  of  capil- 
laries. The  connective  tissue  cells  in  marrow  are  the  marrow  cells 
which  are  concerned  in  bone  formation.  In  yellow  marrow,  the  mar- 
row cells  have  been  replaced  by  fat  cells.  In  addition  there  an-  to 
be  found  in  marrow  some  lame  connective-tissue  cells — the  giant 
cil's — which  are  concerned  in  the  absorption  of  calcified  tissue  and 
which  are  known  under  the  term  of  osteoelasts.  With  the  ex- 
ception of  the  bones  of  the  vault  of  the  cranium,  of  the  face,  and 
part  of  the  lower  jaw.  the  skeleton  is  mapped  out  in  its  fetal  con- 
dition by  solid  cartilage  of  the  hyaline  type.  \Yhen  bone  de- 
velops from  centers  of  ossification  in  cartilage  it  is  known  as 
endochondral  bone.  When  formed  directly  under  the  perios- 
teum it  is  known  as  periosteal  bone.  The  changes  evident  in  en- 
dochondral bone  formation  consist  in  an  increase  in  the  size  of 
the  cartilage  cells,  their  rearrangement  in  rows,  and  an  increase 
in  the  size  of  intercellular  substance  and  the  deposition  of  lime 
salts.  In  endochondral  bone  formation  the  process  is  one  of  sub- 
stitution: namely,  the  cartilage  cells  are  absorbed  and  replaced 
by  new  bone.  In  periosteal  bone  formation  the  process  is  car- 
ried out  through  the  agency  of  the  osteoirenetic  layer.2 


-This    histological    description    of   bone   lias    been   compiled    from    the   writings    of   G.    A. 
Piersol    (Textbook   of  Normal   Histology). 


BONE  457 

Bone  Involvement  in  Dentoalveolar  Abscess 

If  a  section  of  the  mandible  be  examined  it  will  be  found  that 
it  is  composed  of  thick  layers  of  compact  bone  externally  and  in- 
ternally and  thai  within  the  layers  of  compact  bone  the  cancellated 
or  spongy  bone  is  found  (Figs.  357,  358,  359,360,361,362  and  363). 

The  latter  is  made  up  of  the  thin  bony  walls  of  the  cells 
which  contain  the  medullary  or  myelitic  substance,  the  so-called 
cancellated  spaces.  In  life  these  cells  are  not  exactly  spaces,  be- 
ing  almost  entirely  filled  up  by  the  myelitic  substances.  The  char- 
acter of  the  bone  in  the  walls  is  identical  with  that  of  the  compact 
layer  which  surrounds  the  mandible  in  all  of  its  aspects  except 
at  the  upper  aspect  through  which  retention  is  afforded  to  the 
teeth.  The  walls  of  the  alveoli,  internally,  appear  more  or  less 
smooth  and  are  made  up  of  a  layer  of  compact  bone,  although 
everywhere  as  seen  in  ground  sections  examined  microscopically, 
cancellated  spaces  open  through  it.  Not  infrequently  some  such 
cancellated  space  will  be  located  on  a  line  with  a  root  canal,  and 
consequently  when  a  root  canal  instrument  is  forced  past  the 
apical  foramen  it  will  penetrate  for  a  distance  without  finding 
any  obstruction  in  its  way.  The  alveoli  are  supported  by  layers 
of  compact  bone  which  are  the  w  alls  of  the  cancellated  spaces  and 
are  so  arranged  as  to  afford  the  greatest  possible  support  against 
direct  and  lateral  stress  upon  the  teeth. 

In  the  maxilla  there  is  likewise  a  cortical  layer  made  of  com- 
pact bone  buccally  and  lingually,  the  alveoli  of  the  teeth  being 
embedded,  so  to  speak,  in  the  spongy  bone  between  the  cortical 
layers.  The  alveoli  here,  as  in  the  mandible,  are  lined  internally 
by  a  semi-compact  bone  into  which  open  many  of  the  cancellated 
spaces. 

Infections  of  the  periapical  tissues  invariably  lead  to  varied 
degrees  of  involvement  of  the  surrounding  bony  structure.  The 
pathologic  process  which  originates  within  the  alveoli,  spreads 
to  the  cancellated  substance  of  the  jaw,  exhibiting  the  character- 
istics of  an  osteomyelitis,  but  with  no  tendency,  except  rarely,  to 
spread  (Figs.  357,  358  and  359).  Ostcom  yel  it  is  is  a  destructive 
process   affecting    the    periosteum,    the    cortex   and    the   marrow? 

The  cortical  bone  lining  the  alveoli  soon  breaks  clown  as  the 
result  of  the  spreading  of  an  infectious  process  in  the  peridental 

3McCallum:     A  Textbook  of  Pathology,  New  York,  Wm.  Wood  &•  Co. 


458 


DENTAL   PATHOLOGY 


membrane,  and  upon  the  establishment  of  a  passage  through  the 
cortical  layer  at  any  particular  point,  the  infection  reaches  the 
cancellated  substance  of  the  alveolar  walls  which  is,  of  course, 
continuous  with  the  cancellated  substance  of  the  jaw  proper. 
The  absorption  of  the  cortical  bone  of  the  alveoli  in  the  course 
of  an  infectious  inflammation  is  probably  due  to  the  combined  ac- 
tion of  osteoclasts  and  of  leucocytes,  it  having  been  satisfactorily 
shown  by  a  number  of  investigators  that  the  presence  of  osteo- 
clasts is  not  essential  to  the  absorption  of  bone  (Ribbert).4 


Fig.  357. — Alveolar  bone  in  the  periapical  region.  The  section  was  obtained  from  the 
alveolar  bone  around  the  apex  of  the  root.  The  lamellae  of  bone  (calcification  install- 
ments)   are   easily   observed,   also   the    lacunas   or   bone   cell   spaces. 

The  medullary  or  myelitic  substance  in  the  cancellated  spaces 
becomes  the  seat  of  an  inflammation.  Through  osteoclastic  and 
leucocytic  action,  as  previously  noted,  the  hard  substance  of  the 
bone,  viz.,  the  walls  of  the  cancellated  spaces,  disappear;  they 
are,  so  to  speak,  eaten  through,  and  the  Haversian  canals  are 
made  wider.  The  contents  of  the  spaces,  viz.,  the  myelitic  sub- 
stance, become  the  seat  of  an  acute  inflammation  in  which  the 
cellular  elements  typical  of  this  form  of  inflammation  are  present. 
In   time  the   inflamed  medullary  substance,   as   the  result  of  the 


*Adami   and   McCrae:     Textbook  of  Pathology,   Philadelphia,   l.ea  &   Febiger. 


BONE 


459 


big.  358. — Transverse  section  of  tooth  showing  the  arrangement  of  bone  in  the  alveoli 
The  peridental  membrane,  it  will  be  seen,  joins  with  the  medullary  substance  in  the  can- 
cellated spaces;  a,  a,  dentin;  b,  b,  cementum;  c,  c,  peridental  membrane;  d,  d,  d,  d  section 
ot  compact  bone  lining  alveolus;  c,  junction  of  peridental  membrane  with  myeloid  sub- 
stance. 


460 


DENTAL    PATHOLOGY 


K 

,.- 

N# 

i 

■ 

' 

•< 

•.         *.                                            • 

"{"■'*?                                                              /fc 

3r^^~r'iS^     <  -■    alii 

Fig.    359. — Arrangement    of    cancellated    bone    in    region    of    central    incisors. 


Fig.  360. — Bone  of  alveolar  process  and  two  cancellated  spaces.  a,  a,  a,  areas  of 
compact  bone  in  the  cortical  layer  of  an  alveolus;  b,  cancellated  spaces;  c,  c,  peri- 
dental membrane. 


BOXE 


461 


action  of  the  Liquefying  bacterial  toxins,  breaks  down.     In  some 
places  the  cortical  layer  of  the  alveoli  is  less  than  one-third  of  a 


Fig.   361. — Arrangement  of  bone  in  incisal   region,   showing  at  a,  bone  of  alveolar  septum 
between    upper    central    incisors. 


Fig.  362. — Arrangement  of  bone  in  bi- 
cuspid region  showing  at  b,  bone  of  alveo- 
lar  septum    between    the    upper    bicuspids. 


Fig.   263. — Arrangement  of  bone   in   mo- 
lar  region,   showing  at   c,   bone   of   alveolar 

septum    between    upper    molars. 


millimeter  in  thickness.     Its  involvement   and  disappearance  in 
the  direction  of  thickness  is  therefore  quickly  brought  about,  thus 


402  DENTAL    PATHOLOGY 

opening'  an  abundance  of  pathways  for  the  absorption  of  bacteria 
and  bacterial  toxins. 

Acute  or  chronic  apical  infections  can  not  therefore  be  regarded 
from  the  viewpoint  of  localized  infections.  If  all  acute  or  chronic 
infections  of  the  periapical  tissues  do  not  give  rise  to  systemic 
manifestations,  it  is  not  because  the  products  of  such  infections 
are  not  in  all  cases  at  the  portals  of  absorption,  hut  because  the 
individual  is  able  to  combat  successfully  the  bacterial  invasion. 
It  is  purely  a  question  of  individual  resistance  or  immunity  to 
infection. 

Various  chains  of  streptococcus  and  staphylococcus  seem  to  be 
the  predominating  bacteria  in  these  lesions,  although  other  or- 
ganisms may  bring  about  the  same  results  in  association  with  the 
staphylococcus  and  streptococcus,  viz..  the  pneumococcus,  ty- 
phoid bacillus,  and  the  fusiform  bacillus.  The  bacteria  invading 
the  cancellated  spaces  produce  an  inflammation  of  the  medullary 
substance, — a  myelitis.  The  cells  of  the  medullary  substance 
around  the  focus  of  infection  are  destroyed  and  their  places 
taken  by  leucocytes  which  liquefy  the  necrotic  tissues  and 
attack  the  bony  lamellae  which  they  reduce  to  fragments.5 

Necrosis,  Caries  and  Rarefying  Osteitis  of  the  Alveoli  and  of  the 
Jaws.     Necrosis  of  the  Apical  Areas  of  Roots 

Necrosis  is  a  term  applied  to  the  death  of  an  area  of  bone  tissue 
which  is  immediately  surrounded  by  living  cells.  It  is  death  of 
bone  en  masse.  It  implies  the  contemporaneous  death  of  a  large 
number  of  cells  and  their  subsequent  separation  from  the  sur- 
rounding healthy  bone  following  an  inflammatory  process  in- 
augurated in  the  surrounding  healthy  bone.  It  is  distinguished 
from  the  process  designated  as  rarefying  osteitis,  osteoporosis,  or 
caries,  in  that  in  the  case  of  the  latter  the  individual  cells  die 
successively.  Caries  is  a  term  applied  to  the  molecular  de- 
struction of  bone  "corresponding  to  the  ulceration  of  soft  parts."0 

In  caries  both  the  calcified  structure  and  the  organic  matrix 
disappear,  the  former  through  osteoclastic  activity,  the  latter 
through  the  action  of  peptonizing  bacterial  toxins  or  by  the 
discharge  of  peptonizing  enzymes  from  the  leucocytes,  or  by  both. 


BMcCallum:     A  Textbook  of  Pathology. 

r,Stengel  and  Fox:     A  Textbook  of  Pathology.   Philadelphia,   \\*.    B.    Saunders   Co. 


i5o.ni:  4(>:5 

The  causes  of  necrosis  are  all  those  which  directly  or  indirectly 
interfere  with  the  blood  circulation  in  bone.    They  may  be  grouped 

as   follows  : 

1.  Mechanical     Blows,  accidental   traumatism. 

2.  Physical — Extreme  degrees  of  temperature. 

3.  Chemical — (a)  Burns  by  acids,  strong  alkalies,  ar- 
senic trioxide  phenol,  formaldehyde,  etc. 

(b)    The   administration  beyond   the   individual's  tol- 
erance of  mercury,  phosphorus,  and  bismuth. 

4.  Bacteria]  causes — Infections;  viz.,  action  of  bacteria 
and  bacterial  toxins  and  formation  of  bacterial  em- 
boli and  infarcts. 

Necrosis  follows  the  obstruction  of  the  blood  supply,  the  re- 
sult of  the  occlusion  of  a  main  artery  by  an  embolus,  thrombic  or 
infectious.  The  part  dies  without  its  cells  undergoing  a  progres- 
sive degeneration.  The  infectious  emboli  play  a  leading  part  in 
necrosis  of  the  jaws  caused  by  peridental  infections — dentoalveo- 
lar  abscess,  acute  and  chronic.  Masses  of  bacteria  occlude  a 
series  of  capillaries  and  result  in  the  formation  of  infarcts  in  a 
territory  adjacent  to  or  slightly  removed  from  the  infected  tooth 
root. 

Mechanical  Causes. — In  this  group  are  included  causes  which  in- 
terfere with  the  blood  supply  and  which  result  from  degrees  of  vio- 
lence to  the  jaws.  It  is  well  to  bear  in  mind  that  necrosis  in 
the  case  of  bone,  and  gangrene  in  the  case  of  soft  tissue,  results 
from  disturbance  of  circulation  whereby  the  cells  do  not  re- 
ceive the  necessary  amount  of  blood  or  are  not  properly  drained, 
or  from  disturbances  in  the  cells  which  prevent  them  from  as- 
similating  the  required  amount  of  food  even  though  available  in 
normal  quantity  and  quality.  A  blow  in  the  mouth  may  result 
in  such  an  impact  upon  the  vessel  supplying  the  peridental  mem- 
branes of  several  teeth  as  to  result  in  the  cutting  off  of  the  blood 
supply  by  emboli,  with  death  of  the  teeth  and  eventually  their 
exfoliation,  and  in  the  death  of  portions  of  the  surrounding  bony 
areas  following  the  formation  of  occluding  thrombi  in  the  injured 
vessels. 

In  the  group  of  mechanical  causes  are  also  included  the  necro- 
sis and  exfoliation  of  sections  of  the  alveolar  plate  following 
such  accidents  as  falls,  blows,  fractures  during  an  extraction,  etc. 


464  DENTAL   PATHOLOGY 

Chemical  Causes. — Necrosis  of  the  alveolar  bone  is  occasionally 
the  result  of  destruction  of  masses  of  cells  by  the  action  of  chemi- 
cal agents.  The  soft  tissues  of  the  mouth  are  likewise  liable  to 
destruction  by  this  means,  particularly  following  the  use  of  ar- 
senic in  the  devitalization  of  teeth.  In  the  event  that  arsenic 
leaks  out  from  a  cavity  the  soft  tissues  are  first  affected,  and  then 
the  underlying  bone.  Necrosis  of  the  deeper  osseous  structure 
of  the  jaws,  following  the  injudicious  use  of  arsenic  trioxide,  also 
occurs.  Unnecessarily  large  amounts  of  arsenic  in  contact  with 
the  pulp  will  lead  to  that  result.  Too  much  care  can  not  be  ex- 
ercised in  the  use  of  this  chemical  for  purposes  of  devitalizing 
the  pulp,  particularly  so  in  the  case  of  teeth  whose  roots  are  not 
completely  developed  so  that  the  apical  foramina  are  large.  The 
injudicious  use  of  phenol,  trichloracetic  acid,  chromic  acid,  sul- 
phuric acid,  phenolsulphonic  acid  or  formalin  (the  last  three  in 
root  canal  therapeutics)  may  cause  necrosis  in  the  periapical 
region. 

The  careless  forcing  of  acid  compounds  and  strong  alkalies 
through  the  apical  foramen  is  a  relatively  common  source  of  de- 
struction of  periapical  alveolar  bony  tissue  immediately  surround- 
ing the  apex  of  the  root. 

Necrosis  of  the  maxillary  bones  occurs  in  those  under  a  mer- 
curial regime  and  in  persons  engaged  in  the  manufacture  of 
phosphorus  matches.  Those  with  carious  teeth  and  diseased  gums 
are  particularly  liable  to  the  form  of  necrosis  caused  by  phos- 
phorus fumes.  It  was  of  frequent  occurrence  in  the  early  days 
of  the  manufacture  of  phosphorus  matches.  At  the  present  time, 
owing  to  the  care  which  is  given  to  the  teeth  and  gums  of  the  men 
employed  in  this  industry,  the  occurrence  of  phosphorus  necrosis 
has  been  greatly  reduced. 

Bacterial  Causes. — In  this  group  is  included  the  most  frequent 
source  of  tissue  destruction  in  the  roots  of  teeth  and  the  support- 
ing alveolar  structures.  An  apical  abscess,  acute  or  chronic,  may 
cause  a  destruction  of  peridental  fibers  which  is  followed  by  nec- 
rosis of  that  portion  of  the  root  which  is  denuded  of  peridental 
membrane,  or  in  which  the  peridental  membrane  has  undergone 
retrograde  metamorphosis.  The  process  which  takes  place  in  the 
root  following  destruction  of  the  peridental  membrane  is  not 
exactly  typical  of  necrosis,  i.e.,  death  en  masse,  for  the  reason  that 


BONE 


465 


the  cementum  being  devoid  of  a  blood  supply  of  its  own  is  no1  sub- 
ject to  sequestrum  formation,  [nstead  it  undergoes  a  molecular 
disintegration  equivalent  to  bone  caries,  and  manifests  itself  by 
the  condition  so  frequently  diagnosed  as  pathologic  root  resorp- 
tion (Pigs.  364  to  367).    The  process  which  occurs  in  the  alveolar 


Fig.  364. — Resorption  of  the  apical  areas 
of  the  root  of  a  lower  molar  consequent 
upon  chronic  dentoalveolar  abscesses  (den- 
tal   granulomata)    of    long   standing. 


Fig.  365. — Resorption  of  the  roots  of  a 
lower  right  first  molar  consequent  upon  a 
chronic  infection  of  the  periapical  peri- 
dental membrane,  the  sequela  of  a  septic 
pulpitis. 


Fig.  3t'6. — Beginning  of  resorption  of 
the  apical  third  of  a  root  of  an  upper  cen- 
tral following  necrosis  of  the  apical  area 
of  the  root  consequent  upon  a  chronic 
dentoalveolar    abscess. 


Fig.  3f>7. — A  chronic  alveolar  abscess 
(dental  granuloma)  in  the  lower  right 
cuspid,  right  central  incisor,  left  central 
incisor  and  left  cuspid.  The  apices  of 
the  roots  of  the  central  incisors  have  un- 
dergone   marked    resorption. 


osseous  tissue  in  chronic  dentoalveolar  abscess  typifies  tissue 
death  by  consecutive  disintegration  of  cellular  elements  through 
rarefying  osteitis,  osteoporosis  or  caries,  practically  synony- 
mous terms;  or  in  other  words,  gradual  cell  death,  as  already 


4GG 


DENTAL    PATHOLOGY 


described  in  the  case  of  osteomyelitis  leading  to  rarefying  ostei- 
tis, or  to  the  more  complete  process  of  hard-tissue  resorption  with 
liquefaction  of  the  organic  hone  matrix — caries  of  bone  (Fig. 
368).  Necrosis  of  areas  of  alveolar  process  and  jaw  bone  proper 
is  occasionally  observed  in  connection  with  ulcerative  stomatitis. 
The  periosteum  at  the  crest,  or  alveolar  border,  becomes  involved, 


Fig.  368. — Chronic  dentoalveolar  abscess  (dental  granuloma)  of  very  long  standing  in 
which  the  chronic  osteomyelitis  which  developed  in  the  alveolar  process  resulted  in 
caries  of  hone  in  a  relatively  large  area.  The  apex  of  the  tooth  was  found  to  penetrate 
into    a   cavity    in    the    cancellated    substance    of    the    maxilla. 


the  infection  brings  about  its  detachment,  and  the  involvement 
of  the  myeloid  substance  in  the  cancellated  spaces  follows.  The 
blood  supply  is  cut  off  from  the  periosteal  side  and  infectious 
emboli  obstruct  any  number  of  capillaries  in  the  cancellated 
substance,  with  necrosis  as  the  result. 


CHAPTER   XXXVI 

PERIOSTITIS  OF  THE  JAW 

Inflammation  of  the  periosteum  of  the  jaw  may  be  acute  or 
chronic,  depending  on  the  vital  resistance  of  the  patient  and  the 
virulence  of  the  infecting  organism.     The  mosl    frequent  causes 

of  periostitis  of  the  jaws  are: 

1.  Acute  or  chronic  dentoalveolar  abscess. 

2.  Traumatic  injuries  with  or  without  a  communicating  ex- 
ternal wound. 

3.  Chemical  irritation  such  as  may  be  induced  by  the  continued 
use  of  mercury  or  the  inhalation  of  vapors  of  phosphorus. 

4.  As  a  sequence  or  in  the  course  of  acute  or  chronic  systemic 
infections. 

5.  As  a  sequence  to  the  eruptive  fevers  and  anemia  in  children. 
G.  As  the  result  of  tuberculosis  or  syphilis. 

The  acute  form  of  periostitis  may  be  traumatic  or  infectious, 
although  the  traumatic  form,  by  establishing  areas  of  decreased 
vital  resistance  in  the  periosteum,  soon  becomes  infectious, 
through  bacteria  gaining  access  by  the  hematogenic  route  in  the 
case  of  traumatism  without  external  communicating  injuries,  or 
from  the  outside  in  the  case  of  traumatisms  accompanied  by  ex- 
tensive breaks  in  the  continuity  of  the  soft  tissues. 

In  the  chronic  infectious  periostitis  in  which  the  bacteria  are 
of  low  virulence,  thickening  of  the  periosteum  with  new  bone 
formation  in  the  form  of  osteophytes  and  nodular  formations,  oc- 
curs wherever  the  osteogenetic  layer  is  stimulated,  but,  of  course 
not  where  the  cells  are  undergoing  degeneration.  The  infectious 
or  suppurative  form  of  acute  periostitis  may  or  may  not  lead  to 
necrosis  of  the  underlying  bone.  If  the  infected  area  is  speedily 
drained  by  a  sinus,  or  following  surgical  interference,  necrosis 
will  not  occur:  but  if  the  reverse  should  be  the  case,  necrosis  will 
result.  The  infectious  inflammation  is  intraperiosteal  or  sub- 
periosteal, or  both.  In  the  event  that  no  drainage  through  the 
periosteum  is  established,  the  inflammation  proceeds  between  the 
periosteum   and  the  bone,   strips  the  latter  of  its  overlying  peri- 


468 


DENTAL   PATHOLOGY 


osteum,  and  necrosis  of  the  superficial  layers  of  bone  follows. 
The  infection  may  then  penetrate  back  into  the  cancellated  spaces 
wherein,  as  the  result  of  multiple  infectious  emboli  (occlusion  of 
arterioles  and  capillaries),  interference  of  the  circulation  takes 
place,  resulting  in  more  extensive  areas  of  necrosis  than  where 
the  periosteum  alone  is  affected.  Dentoalveolar  abscess  is  a 
frequent  source  of  periostitis  of  the  jaws  accompanied  by  necro- 
sis and  the  formation  of  sequestra  (Fig.  369). 

Acute  periostitis  may  be  localized  or  diffused,  according  to  the 
degree  of  resistance  of  the  tissues  immediately  over  the  path  of  the 


Fig.    369. — Sequestrum   wliicli    came   away   attached   to   a   tooth   following   a   chronic    dento- 
alveolar abscess  of  long  standing. 


infection,  and  the  type  of  microorganism  concerned  in  the  infec- 
tion. A  small  area  of  bone  may  die ;  and  again,  the  process  may 
be  of  a  progressive  character — a  diffuse  acute  periostitis — caus- 
ing the  formation  of  a  number  of  sequestra  over  a  relatively 
extensive  area  of  the  jaw.  An  acute  dentoalveolar  abscess  re- 
sults usually  in  a  localized  acute  periostitis,  which  subsides  upon 
the  removal  of  the  infectious  source  in  the  root  canal.  The  perios- 
tiiis  may,  however,  be  of  the  diffuse  type,  accompanied  by  exten- 
sive necrosis.  Acute  periostitis,  if  diffused,  results  in  secondary 
osteomyelitis,  causing  a  greater  depth  of  necrosis  of  the  jaws  or 


PERIOSTITIS    OF    THE    .1  \\\  409 

caries  of  bone.  It  occurs  with  greater  frequency  in  the  lower  than 
in  the  upper  jaw,  by  reason  of  the  Ead  thai  in  the  upper  the  blood 
supply  is  more  abundant  and  anastomosis  of  blood  vessels  is 
greater  than  in  the  lower.  Periostitis  is  more  frequenl  in  chil- 
dren and  young  persons,  inasmuch  as  it  is  during  childhood  and 
early  maturity  that  there  is  greater  susceptibility  to  dental 
caries  (a  prolific  source  of  periostitis)  by  reason  of  involvement 
of  the  pulp,  and  later  of  the  peridental  membrane. 

The  infection  may  spread  from  a  root  canal  into  the  can- 
cellated substance  of  the  jaws  and  then  into  the  periosteum 
where  it  sets  up  an  acute,  though  limited  infection.  The  symp- 
toms of  such  a  periostitis  are  as  a  general  rule  attributed  to  the 
infectious  process  in  the  peridental  membrane  and  periapical 
structures — the  acute  dentoalveolar  abscess.  The  symptoms  are 
masked  by  the  pain  incident  to  the  inflammation  of  the  peridental 
membrane  and  the  osteomyelitis  in  the  alveolar  bone.  If  the 
periosteum,  at  the  point  through  which  the  infection  passes,  were 
to  be  examined,  it  would  be  found  red  and  swollen  and  the  area 
around  the  opening  to  be  the  seat  of  an  infiltration  by  polymor- 
phonuclear leucocytes,  some  lymphocytes,  and  by  serum  and 
Lymph.  Sometimes  the  area  of  periosteum  is  infiltrated  with 
blood.  A  periapical  infection  leading  to  a  dentoalveolar  abscess 
with  involvement  of  the  cortical  and  cancellated  substance  of  the 
jaw  and  the  soft  tissues  of  the  face,  induces  a  periostitis  in 
all  cases.  The  opening  through  the  external  cortical  plate 
of  the  alveolus  into  the  soft  tissues  marks  the  location  of  the 
area  of  periostitis.  The  infection  persisting  even  in  a  mild  de- 
gree, regeneration  of  the  periosteum  is  prevented  and  the  chan- 
nel leading  from  the  focus  of  infection  to  an  external  opening- 
persists  until  such  time  as  the  source  of  the  infection  is  completely 
removed,  and,  in  abscesses  of  long  standing,  until  the  rarefied  area 
as  the  result  of  rarefying  osteitis  and  bone  caries  is  curetted  and 
mildly  stimulated  to  fill  up  the  loss  of  osseous  tissue.  The  reten- 
tion of  pus  subperiosteal^  is  responsible  for  the  death  (necrosis) 
and  exfoliation  of  one  or  more  sequestra.  Periostitis  of  the  jaws 
may  be  preceded  by  osteomyelitis,  or  vice  versa.  In  the  case  of  a 
spreading  pericemental  infection  resulting  in  a  periostitis,  acute 
and  of  short  duration,  or  in  chronic  periostitis  when  the  inflamma- 
tory exudates  become  incarcerated  under  the  periosteum,  the  peri- 


470  DENTAL    PATHOLOGY 

ostitis  has  been  preceded  by  infectious  processes  in  the  substance 
of  the  bone  involving  the  osseous  and  medullary  substances,  viz., 
an  osteomyelitis.  Again  if  the  pus  finds  no  outlet,  owing  to  the 
resistance  of  the  periosteum,  the  infection  may  penetrate  back 
again  into  the  bone  through  the  cortical  layer,  causing  a  more  ex- 
tended osteomyelitis  leading  to  more  extensive  rarefying  osteitis, 
bone  caries,  or  necrosis. 

The  commonest  form  of  chronic  periostitis  is  that  of  syphilitic 
origin.  Growth  of  bone  through  stimulation  of  the  osteogenetic 
layer  occurs.  The  inflammation  must  be  mild  and  continuous  in 
character  in  order  to  result  in  new  bone  formation.  It  can  not, 
of  course,  occur  where  the  cells  of  the  osteogenetic  layer  have 
undergone  degeneration,  but.  on  the  other  hand,  it  does  take 
place  in  areas  beyond  those  of  degeneration  in  which  the  effect 
of  the  infection  does  not  overbalance  stimulation. 

In  chronic  phosphorus  poisoning,  periostitis  of  the  noninfec- 
tious type  develops  at  first,  but  remains  as  such  only  a  short  time. 
The  irritation  caused  by  the  phosphorus  fumes  lowers  the  re- 
sistance of  the  periosteum  and  this  becomes  the  seat  of  bacterial 
proliferation  with  its  sequelae.  Fever;  general  indisposition: 
swelling  of  the  gums  and  face  on  the  affected  side ;  looseness  and 
exfoliation  of  the  teeth;  pus  discharges  from  around  the  necks 
of  the  teeth:  trismus;  sinus  or  sinuses,  intra-oral  or  extra-oral — 
are  some  of  the  most  salient  symptomatic  manifestations  of  perios- 
titis of  the  jaws. 

OsU  itis  is  an  inflammation  of  the  bone  leading  to  either  rare- 
faction or  condensation  involving  the  cancellated  and  compact 
substance  of  bone.  Osteomyelitis  affects  both  the  calcified  tissue 
and  the  medullary  substance.  Osteitis  and  myelitis  invariably  go 
together.  In  the  rarefying  form  the  inflammation  of  the  medul- 
lary substance  brings  about  osteoclastic  activity,  and  disappear- 
ance of  particles  of  calcified  tissue  follows,  giving  the  bone  a 
honeycomb  appearance.  Karefying  osteitis  is  a  chronic  process. 
The  erosions  on  an  area  of  bone  undergoing  rarefying  osteitis 
are  called  Howship's  lacuna,  in  which  osteoblasts  and  giant-cells 
(osteoclasts)  are  to  be  seen  together. 


CHAPTER  XXXVI] 
PYORRHEA  ALVEOLARIS 

Historical  Sketch 

An  examination  of  ancienl  skulls  leads  to  the  belief  that  the 

earlier  races  were  subject  "to  diseases  of  the  investing  tissues  of 
the  teeth  which  are  very  closely  allied  in  pathologic  characteris- 
tics to  the  pyorrhea  alveolaris  of  modern  limes.  The  lesions  of  the 
alveolar  process  to  he  seen  in  many  specimens  seem  to  confirm 
the  opinion  held  by  most  writers  on  the  subject  that  pyorrhea  al- 
veolaris. or  some  other  disease  leading  to  the  exfoliation  of  the 
teeth,  dates  almost  as  far  back  as  the  human  race.  Under  the 
term  "scurvy  of  the  gums"  Pierre  Fauchard,  in  1746,  described 
a  lesion  of  the  gums  beyond  the  power  of  therapeutic  means  to 
eradicate  and  which  invariably  terminated  in  the  loss  of  the 
teeth.1 

In  1778  Jourdain,  in  his  treatise  on  diseases  of  the  mouth,  de- 
scribes pyorrhea  alveolaris  under  the  name  of  "suppuration  con- 
jointe  des  alveoles  et  des  gencives,"  namely,  a  simultaneous  sup- 
puration of  the  alveoli  and  gums.  Toriac,  in  1823,  seems  to  have 
been  the  first  writer  to  suggest  the  word  "pyorrhea,"  he  having 
named  the  disease  "pyorrhee  inter-alveolo-dentaire."  The  term 
was  first  used  by  him  on  the  occasion  of  an  oral  communication 
to  a  medical  society  of  Paris.2 

Oudet,  in  1835,  recognized  the  peridental  membrane  as  the  seat 
of  the  disease,  and  Marechal  de  Calvi,  in  1861,  described  pyorrhea 
alveolaris  with  perhaps  more  clearness  than  any  one  of  his  pred- 
ecessors in  the  field,  and  named  it  "expulsive  gingivitis."  Thos. 
Pell',  in  1829,  recognized  two  forms  of  the  disease:  one  of  local 
origin  with  deposits  as  the  exciting  cause;  the  other  of  constitu- 
tional origin.  Chapin  A.  Harris,  in  18,53,  in  his  work,  "Principles 
and  Practice  of  Dental  Surgery,"  describes  the  disease  under 
consideration  under  the  heading  of  "Chronic  Inflammation  and 


'Fauchard,   Tierre:      Chirurgien   dentiste,    1746,   i. 

2Frey,    Leon:      Pathologic   des-Dentes  et   de   la   Bouche. 

'Marshall,   J.    S.:      Operative    Dentistry,    Philadelphia,   J.    B.    Uppincott    Co. 

471 


472  DENTAL   PATHOLOGY 

Tumefaction  of  the  Gums  Attended  by  Recession  of  Their  Mar- 
gins from  the  Teeth."  Harris  recognizes  a  lo<?al  as  well  as  a 
systemic  cause.  He  says  that  chronic  inflammation  of  the  gums 
may  exist  for  years  without  being  attended  by  suppuration  or 
recession  of  their  margins  from  the  necks  of  the  teeth ;  but  that, 
sooner  or  later,  according  to  the  amount  of  local  irritation  and 
the  state  of  the  constitutional  health  and  habit  of  the  body,  these 
phenomena  are  developed.  With  the  occurrence  of  inflamma- 
tion the  margins  of  the  gums  gradually  lose  their  festooned  ap- 
pearance, become  thick,  spongy  and  rounded;  and  ultimately,  on 
being  pressed,  purulent  matter  is  discharged  from  between  them 
and  the  necks  of  the  teeth.  The  sensibility  is  increased  and  they 
bleed  from  the  most  trifling  injury.  He  describes  the  possibility 
of  constitutional  symptoms  developing  as  the  result  of  a  local  in- 
fection, saying  that  "more  vital  organs  become  implicated  and 
the  health  of  the  general  system  is  sometimes  very  seriously  im- 
paired." In  1867  Magitot,  of  Paris,  published  his  views  on  pyor- 
rhea alveolaris,  designating  the  disease  by  the  term  "osteo- 
periostite  alveolo-dentaire,"  and  disregarding  the  role  played  by 
calcareous  deposits  in  the  production  of  the  disease.  As  the 
antithesis  of  Magitot's  writings,  those  of  John  W.  Riggs  of 
Hartford,  Conn.,  appeared  in  1875.  Riggs,  after  whom  pyorrhea 
alveolaris  is  today  designated  by  some  authors  as  Riggs'  disease, 
described  the  disease  as  a  suppurative  inflammation  of  the  gums 
with  absorption  of  the  gums  and  alveolar  processes,  and  he  at- 
tributed the  disorder  to  local  causes.  Dr.  F.  H.  Rehwinkel,  in 
1877,  called  attention  to  the  possibility  of  pyorrhea  alveolaris 
developing  in  the  absence  of  local  factors,  and  also  said  that  it 
is  a  hereditary  and  constitutional  disease.  Dr.  fi.  V.  Black,  whose 
investigations  of  pyorrhea  alveolaris  appeared  in  1866,  discussed 
it  almost  exclusively  from  the  local  standpoint — a  destructive  in- 
flammation of  the  peridental  membrane.  Among  the  most  im- 
portant contributors  since  then  to  the  etiology  and  pathology  of 
pyorrhea  alveolaris,  the  names  of  Miller,  Kirk,  Talbot,  Darby, 
Truman,  Rhein,  Hartzell,  Hopewell-Smith,  Ottolengui,  and  R.  R. 
Andrews,  stand  out  conspicuously.  The  investigations  by  Kirk 
on  the  relation  of  faulty  metabolism  to  pyorrhea  alveolaris  and 
pericemental  abscess  of  gouty  origin,  constitute  a  series  of  most 


PYORRHEA    ALVEOLARIS  473 

valuable  contributions,  which  the  studenl  of  the  subbed  should 
consult4. 

General  Considerations 

The  term  "pyorrhea  alveolaris"  is  generally  accepted  as  in- 
dicative of  inflammatory  disorders  in  the  in/vesting  tissues  of 
Hie  t<<th,  which  if  not  controlled,  eventually  end  in  their  ex- 
foliation. The  true  meaning  of  the  term  is  "flow  of  pus  from 
the  alveolus,"  and  inasmuch  as  destruction  of  the  peridental 
membrane  and  alveolar  bone,  which  results  in  the  loss  of  the 
teeth,  is  not  always  attended  by  a  visible  flow  of  pus,  the  term 
pyorrhea  alveolaris  is  often  incorrectly  applied  so  far  as  true 
pathologic  significance  is  concerned.  The  loosening  and  ac- 
tual loss  of  a  tooth  is  the  result  of  the  destruction  of  prac- 
tically all  of  the  peridental  membrane  and  adjacent  alveolar 
bone ;  and  it  thus  happens  that  all  pathologic  conditions  in  these 
structures,  as  well  as  in  the  overlying  gum  tissues,  of  which  the 
prognosis  is  loss  of  a  tooth  by  exfoliation,  these  have  come  to  be 
designated  under  the  generic  term,  "pyorrhea  alveolaris."  Many 
terms  have  been  suggested  as  substitutes  for  this  one,  namely, 
phagedenic  pericementitis,  interstitial  pericementitis,  Kiggs'  dis- 
ease, alveolo-dental  pericementitis,  interstitial  gingivitis,  gouty 
pericementitis,  ptyalogenic  calcic  pericementitis,  dentoalveolitis, 
pyodestructive  pericementitis,  etc.  Not  one  of  these  terms, 
however,  depicts  the  series  of  pathologic  phenomena  more  clearly 
than  the  commonly  employed  term,  pyorrhea  alveolaris,  and  con- 
sequently no  change  in  the  nomenclature  seems  justifiable  at  this 
time,  at  least  in  favor  of  any  of  the  previously  mentioned  names. 

Clinically,  several  forms  of  pyorrhea  alveolaris  are  distinguish- 
able. In  one  form  the  destructive  inflammation  in  the  peridental 
membrane  and  alveolar  process  is  preceded  by  varying  degrees  of  ir- 
ritation to  the  gingiva?  by  salivary  calculi;  in  another,  subgin- 
gival calculi  are  the  source  of  irritation  to  the  structures  in- 
volved in  the  inflammatory  process.  The  etiology  of  the  latter 
form  of  calcareous  deposits  has  been  studied  in  a  preceding 
chapter.  Therefore,  suffice  it  to  say  at  this  time  that  subgingival 
deposits  do  not  occur  unless  the  gingiva  have  been  subjected 


4Arthritism    bv    E.    C.    Kirk.    Dental    Cosmos,    July,    1909. 
•Abscesses   Upon   Teeth   with   Living-   Pulps,   Dental   Cosmos.   1898. 
Pericemental  Abscess,   Dental  Cosmos,   1900. 


474  DENTAL   PATHOLOGY 

for  some  time  to  irritating  stimuli ;  that  weak,  insufficient,  or  flat 
approximal  contacts,  the  rough  edges  of  crown-bands,  of  im- 
perfectly inserted,  fillings,  or  any  other  form  of  mechanical  irrita- 
tion; or  that  chemical  irritation  which  develops  consequent  upon 
the  decomposition  of  food,  debris  and.  of  the  slimy  coatings  next 
to  the  gingivae — these  are  among  the  most  prominent  predispos- 
ing causes.  In  all  true  forms  of  pyorrhea  alveolaris  the  bacterial 
factor  is  to  be  viewed  as  the  exciter  of  the  inflammatory  process 
which  causes  the  loss  of  peridental  membrane  and  alveolar  proc- 
ess, and  the  exfoliation  of  the  teeth. 

Pyorrhea  Alveolaris  Caused  by  Salivary  Calculi 

In  the  form  caused  by  salivary  calculi  the  clinical  phenomena 
are  not  typical  of  pyorrhea  alveolaris,  and  while  it  is  here  dis- 
cussed under  that  general  heading,  it  should  be  borne  in  mind 
that  we  consider  that  the  presence  of  pockets  alongside  the  roots 
of  teeth,  which  have  developed  there  consequent  upon  the  de- 
struction of  the  peridental  membrane  and  alveolar  process 
through  bacterial  activity  or  through  vascular  insufficiency  lead- 
ing to  atrophy,  plus  bacterial  activity,  arc  the  essential  phenomena 
of  true  pyorrhea  alveolaris.  The  pathologic  phenomena  accompany- 
ing the  destruction  of  the  investing  tissues  by  salivary  calculi 
are  not  characterized  by  the  formation  of  pockets,  which  if  at  all 
present  are  shallow,  being  not  more  than  two  millimeters  in 
average  depth.  The  peridental  membrane,  alveolar  process,  and 
overlying  gum  tissue  are  destroyed  to  the  level  of  the  salivary 
deposit  as  the  result  of  a  combination  of  pressure  atrophy  and 
bacterial  activity.  Consequently,  in  the  salivary  calculi  form  of 
pyorrhea  alveolaris  (correctly  interpreted,  the  process  should 
be  termed  calcic  gingivitis,  pericementitis  and  alveolitis),  the 
formation  of  pockets  does  not  occur,  and  the  degree  of  suppurative 
inflammation  under  the  deposit,  if  there  should  be  any,  is  not  pro- 
nounced at  any  time.  Pus  forms  at  a  very  slow  rate,  and  it  is 
seen  at  the  junction  of  the  deposit  with  the  soft  tissues,  or  upon 
the  removal  of  the  deposit.  Pus  is  not  by  any  means  invariably 
associated  with  salivary  calculi.  In  those  cases  in  which  it  is 
present,  the  suppurative  inflammation,  in  addition  to  the  phe- 
nomena of  pressure  atrophy,  is  responsible  for  the  destruction 
of  the  investing  tissues ;  while  in  those  cases  in  which  no  evidence 


PYOKKIIKA      UAKOPAPIK 


475 


Fig.  370. — Subgingival  deposits  on  the  root 
surfaces  of  the  lower  central  and  lateral  incisors. 
Destruction  of  the  alveolar  process  and  peri- 
dental membrane  on  the  approximal  surfaces  of 
these  teeth,  resulting  in  the  formation  of  so- 
called    pyorrhea   pockets. 


Fig.  371. — Absence  of  approxi- 
mal contact  accounting  for  the  for- 
mation of  a  pocket  between  lateral 
incisor   and    cuspid. 


Fig.   372. — Absence  of  contact  and  pyor- 
rhea   pocket   formation. 


Fig.  373. — Absence  of  contact  and  pyor- 
rhea  pocket    formation. 


Fig.     374. — Absence     of     contacts 
pyorrhea    pocket    formation. 


and 


Fig.  375. — Absence  of  contact  and  pyor- 
rhea pocket   formation. 


476 


DENTAL    PATHOLOGY 


of  suppuration  is  to  be  detected  the  investing  tissues  are  de- 
stroyed, probably  mainly  as  the  result  of  vascular  interference, 
which  leads  to  atrophy.  The  appearance  of  the  gum  tissues  after 
the  removal  of  a  salivary  calculus  is  that  of  an  ulcerated  surface: 
the  tissues  are  red  and  swollen,  the  inflammation  immediately 
under  the  deposit  being  more  severe  than  in  areas  not  immediately 
in  contact  with  it.  They  bleed  readily,  and  unquestionably  are 
instrumental  in  the  absorption  of  bacteria  and  bacterial  toxines, 
which  are  responsible  for  the  onset  of  systemic  disturbances. 


Fig.  376.— An  area  of  gingiva;,  from  a  pyorrhea  pocket,  the  seat  of  a  chronic  inflamma- 
tion. Longitudinal  section,  a,  a,  stratified  squamous  epithelium  lining  suhgingival  wall; 
/».  /\  />,  epithelial  proliferations,  the  result  of  the  chronic  inflammation  involved  in  the 
tissue;  c,  c,  areas  of  round-cell  infiltration  in  which  the  mononuclear  wandering  cells 
predominate    (leucocytes,    plasma    cells    and    some    mast    cells). 


Pyorrhea  Alveolaris  Caused  by  Subgingival  Deposits 

In  the  form  caused  by  subgingival  deposits  (Fig.  370),  the  de- 
structive inflammation  affects  the  peridental  membrane,  alveolar 
bone,  and  gingiva?;  but  the  gum  tissue  proper,  while  the  seat  of 
;i  chronic  inflammation,  does  not  disappear  or  break  down  simul- 
taneously with  the  peridental  membrane  and  alveolar  process, 
as  is  the  case  in  the  form  caused  by  salivary  calculi.  Following 
octrees  of  irritation  to  the   gingiva'  by  food  impactions  which 


PYORRHEA    ALVEOLARIS 


477 


Fig.  377.— Gum  tissue  overlying  a  pyorrhea  pocket,  decalcified  section.  Little  remains 
to  identify  the  character  of  the  tissue,  the  major  portion  of  which  is  now  substituted  bj 
inflammatory  wandering  cells.  Areas  of  chronic  inflammation  are  seen  throughout  the  t.s- 
~  a  a,  gum  tissue;  b,b,  decalcified  area  of  tooth;  c,  c  pyorrhea  pocket;  d  d 
Gratified  squamous  epithelium  from  gingival  cul-de-sac;  e  c  c,  large  areas  of  round-cell 
infiltration    (predominance    of    mononuclear    wandering    cells). 


478 


DKNTAL   PATHOLOGY 


Fig.  378. — Chronic  gingivitis  in  the  gingiva  which  by  process  of  continuity  will  spri  ad 
to   tin  d    peridental    membrane,      a,  a     cementum;    b,  b,    dentin;    c,c,c,    stratified 

ous    epithelium    lining   gingival    cul-de-sac;    d,    large    area    of    round    cell    infiltra 
(predominance   of   mononuclear   wandering  cells). 


\'\  ORRHEA     \1.\  EOLARIS 


479 


find  lodgmenl  between  the  teeth  in  the  presence  of  either  defec 
tive  approximal  contacts  (Figs.  371,  372,  373,  374,  and  375^,  or 
in  t lio  absence  of  contacts;  by  tiegled  of  the  teeth  through  in- 
sufficienl  brushing,  etc.;  by  the  rough  edges  of  fillings  or  crown 
bands;  by  salivary  calculi;  by  severe  manipulations  of  ligatures 
and  rubber  dam  clamps;  or  by  improper  handling  of  the  tooth- 
brush, producing  injuries  of  the  gingival  margins,  an  inflamma- 
tory process  is  inaugurated  in  these  tissues  (the  Eree  gingiva?)  ac- 
companied by  the  depositions  of  calcareous  masses  thereunder. 


Fig.  379.  Decalcified  transverse  section  of  upper  central  incisor.  In  the  gum  tissue 
;i  chronic  inflammatorj  process  is  going  on  which  has  resulted  in  ana-  of  tissue  liquefac- 
tion. In  this  instance  the  chronic  gingivitis  had  not  as  yet  involved  the  alveolar  process, 
although  eventually  it  will  il"  so.  a.ti.  alveolar  process;  b,  b,  areas  of  tissue  liquefaction 
in  stroma  of  mucous  mfembrane  of  gum  tissue;  c,  cementum;  d,  dentin;  e,  pulp. 


The  subgingival  deposits  thus  produced  irritate  and  subsequently 
bring  about  an  infectious  inflammation  of  the  gingivae,  gums,  and 
later  of  the  peridental  membrane  immediately  adjacent  to  them 
(Figs.  376-382).  Through  the  action  of  Liquefying  bacterial  tox- 
ines  the  peridental  libers  disappear  and  the  infectious  inflamma- 
tion, as  soon  as  the  cresl  of  the  alveolar  process  is  reached,  enters 
the  bone  and  there  sets  up  an  osteomyelitis  with  the  absorption 
of  the  bony  Lamella  (Fig.  383).    The  inflammation  extends  again, 


480 


DENTAL   PATHOLOGY 


Fig.  380. — An  area  of  peridental  membrane  the  seat  of  chronic  inflammation  in  pyor- 
rhea alveolaris.  a,  decalcified  section  of  tooth;  b,b,h.  fibers  of  peridental  membrane  cut 
at  different  angles;  c,c,c,  areas  of  round-cell  infiltration  (predominance  of  mononu- 
clear  wandering  cells). 


PYORRHEA     \l.\  EOLARIS 


181 


Fig.  3M. — Chronic  inflammation  of  peridental  membrane.     Areas  of  tissue  liquefaction 
a,  a.  dentin;  b,  b,  cementum;  c,  c,  c,  fibers  of  peridental  membrane;   </.  d,  alveolar  process; 
c,  c,   areas   of   destruction   of   peridental   fibers    (liquefacti 


482 


DENTAL    PATHOLOGY 


d 


Fig.  382. — Transverse  section  showing  a,  dentin;  b,  cementum;  c.  peridental  mem- 
brane; d,  areas  of  infection  in  the  fibers  of  the  peridental  membrane  which  run 
from  the  cementum  of  one  tooth  to  the  cementum  of  the  adjoining  tooth.  This  picture 
enables  us  to  understand  the  meaning  of  infection  of  the  peridental  membrane  by  con- 
tinuity from  the  gingiva.  At  e,  e,  the  infection  is  seen  progressing  from  the  direction  of 
the    gingiva. 


PYORRHEA     \I.\  EOLARIS 


-]>:; 


Fie     383— An    infection    from    the    peridental    membrane    has    involved    the    medullary 
substance  in  the  cancellated  space,  an  osteomyelitis  being  the  result      a.  decalohed  sect.on 
StoSE   £  6?  peridental    membrane;    c,  c,  c,    alveolar    bone;    d,    chrome    inflammation    in 
llary   substance  of  a  cancellated   space. 


484 


DENTAL   PATHOLOGY 


bringing'  about  the  deposition  of  further  subgingival  deposits 
higher  up  on  the  root  surface,  so  that  the  processes  of  irritation,  in- 
fectious inflammation,  and  bone  resorption  consequent  upon  osteo- 
myelitis, is  repeated;  and  so  on  until  the  entire  peridental  mem- 


Fig.  384. — Destruction  of  alveolar  proc- 
ess and  peridental  membrane  caused  by 
food  impactions  due  to  absence  of  normal 
contact  between  the  upper  left  cuspid  and 
upper  left  first  bicuspid  and  between  the 
latter  tpoth  and  the  upper  left  second  bi- 
cuspid and  between  this  tooth  and  the 
upper    left    first    molar. 


Fig.  385. — Destruction  of  the  alveolar 
process  and  peridental  membrane  in  py- 
orrhea alveolaris,  between  the  upper  right 
cuspid  and  upper  right  first  molar  caused 
by    a    defective    bridge   restoration. 


Fig.  386. — Absorption  of  the  apical  areas  of  the  roots  of  the  upper  central  incisors 
caused  by  an  infection  which  had  originated  at  the  gingival  margin  and  which  had 
caused    a    large    pyorrhea   pocket. 

brane  and  alveolar  process  are  destroyed,  and  the  tooth  is  exfo- 
liated (Figs.  384-401).  In  any  one  of  the  two  forms  of  pyorrhea 
alveolaris  so  far  described  the  presence  of  any  systemic  disorder 
in  the   digestive,   respiratory   or   urinary   tract,    or   any   chronic 


l'YOKKIIKA    ALVEOLARIS 


4S.1 


nervous  disorder,  or  any  systemic  intoxication  of  whatever  origin 
it  mighl   lie.  acts  as  the  means  of  "perpetuating"  the  disease  in 


A  B 

Fig.  3S7. — Two  radiograms  loaned  to  the  author  by  Dr.  T.  A.  Lynch  of  Los  Angeles. 
These  pictures  were  taken  a  few  hours  apart  and  on  account  of  faulty  radiographic 
technic,  B  shows  a  marked  improvement  over  the  pyorrhea!  condition  shown  in  A.  The 
"regeneration"  of  the  alveolar  process  which  is  shown  in  the  picture  on  the  right  side 
is  a  fictitious   result. 


Fig.  388. — Destruction  of  the  alveolar 
process  and  peridental  membrane  caused  by 
a  defective  crown  impinging  upon  the 
gingiva.  By  continuity  the  infection  spread 
to  the  alveolar  septum  bringing  about  its 
partial  destruction.  In  time  a  deep  pyor- 
rhea   pocket    would    result. 


Fig.  389. — Destruction  of  the  alveolar 
process  and  peridental  membrane  resulting 
in  the  formation  of  a  pocket  caused  by  the 
perforation  of  the  distal  wall  of  the  root 
of   an    upper    right   cuspid. 


the  investing  tissues.    The  causes  of  the  pyorrhea  alveolaris  may 
be  of  a  local  character,  but  the  presence  of  systemic  disorders 


486 


DENTAL   PATHOLOGY 


f£-:  it 


jM 


Fig.  390. — Destruction  of  alveolar  process  and 
peridental  membrane  in  pyorrhea  alveolaris  con- 
sequent upon  chronic  osteomyelitis  in  alveolar 
bone. 


ft. 


Fig.  391. — Destruction  of  the  al- 
veolar process  and  peridental  mem- 
brane in  pyorrhea  alveolaris  conse- 
quent upon  chronic  osteomyelitis  in 
alveolar   bone. 


Fig.  392. — Destruction  of  alveolar 
process  and  peridental  membrane  in  py- 
orrhea alveolaris.  A  deep  pocket  existed 
between  the  central  incisors  and  between 
these    teeth   and    the    lateral    incisors. 


Fig.  393. — Destruction  of  alveolar  proc- 
ess and  peridental  membrane  establishing 
a    pocket    distal    to    t he    Inst    molar. 


Fig.  394. — Extensive  pockets  involving 
all  the  roots  of  lower  first  and  second  mo- 
lars. 


Fig.  395. — Extensive  destruction  of  al- 
veolar process  in  pyorrhea  alveolaris. 
Deep  pockets  in  molar  region;  subgingival 
deposits  are  to  be  seen  on  mesial  surface 
of    upper    first    molar. 


PYORRHEA     \l.\  I  OLARIS 


1-7 


makes  it  possible  for  the  disease  to  gain  a  foothold  upon  the  in- 
vesting tissues  such  as  t<>  render  its  eradication  a  problem  beyond 
the  power  of  available  surgical  and  therapeutic  means. 

Pyorrhea  Alveolaris  of  Systemic  Origin 

Any  systemic  disorder  which  produces  alterations  in  the  quan- 
tity or  quality  of  the  blood,  such  as.  for  instance,  Bright's  disease, 
diabetes,  or  the  uric  acid  diathesis,  tuberculosis,  syphilis,  etc., 
may  ad  as  the  systemic  predisposing  causes  of  pyorrhea  alveo- 


Fig.  396. — Pyorrhea  alveolaris.  Destruction  of  the  alveolar  process  and  peridental 
membrane  to  a  depth  of  from  5  to  7  millimeters.  Distal  movement  of  the  affected  teeth 
on  account  of  the  destruction  of  the  peridental  membrane  fibers  which  run  from  the 
peridental  membrane  of  one  tooth  to  that  of  the  other  (transverse  fillers  i.  Malocclusion 
had  been  the  predisposing  cause  of  the  disease  in  this  case.  Observe  the  absence  of  the 
greater  portion  of  the  gingiva  around  the  affected  teeth.  Subgingival  deposits  were  present 
upon   the   mesial,   labial,   and   distal   root   surfaces. 

laris.  These  disorders  are  reponsible  for  the  lowering  of  the  de- 
fensive forces  of  the  body,  and  this  decrease  in  vital  resistance  is 
perhaps  nowhere  more  pronounced  than  in  the  investing  tissues 
of  the  teeth ;  for,  as  pointed  out  by  Talbot,  the  peridental  mem- 
brane, alveolar  bone,  gingiva?  and  gums  are  in  the  nature  of  end- 
organs — devoid,  or  practically  so,  of  collateral  circulation,  and 
consequently  are  markedly  sensitive  to  circulatory  changes. 

These  systemic  derangements  are  to  be  viewed  in  the  light  of 
predisposing  causes.  They  render  possible  the  infection  of  the 
investing  tissues  by  reason  of  their  having  established  in  those 
structures  areas  of  decreased  vital  resistance.    The  bacterial  ex- 


488 


DENTAL    PATHOLOGY 


J'1"-  •> ''■ — Pyorrhea  alveolaris  in  the  lower  teeth  in  the  same  case  as  shown  at  Fig. 
395.  Distal  movement  of  the  affected  teeth.  Considerable  loss  of  alveolar  bone  and  peri- 
dental   membrane    between    the    lower    central    incisors. 


Fig.  39S. — Pyorrhea  alveolaris  in  the  upper  right  cuspid,  first  bicuspid  and  first  molar. 
'  omplete  destruction  of  gingiva  and  destruction  of  alveolar  process  and  peridental 
membrane  for  a  distance  of  several   millimeters. 


l'YORKIIKA     \l.\  EOLARIS 


IS!  I 


eiters  are  of  course  presenl  a1  all  times  in  the  mouth,  and  there- 
fore, following  the  slightesl  break  in  the  continuity  of  the  tissues 
consequent  upon  an  injury  to  the  gingival  structures,  bacteria 
gain  entrance;  and  the  causes  which  made  this  possible  persist- 


Fig.    399.— Pyorrhea   alveolaris.      Subgingival   deposits  were   present   on   the   surface   of  the 
roots   in    relation    with    the    so-called    "pyorrhea   pockets.-' 


Fig.  400. — A  typical  case  of  pyorrhea  alveolaris.  Xote  absence  of  the  septal  gingivae 
and  of  the  body  of  the  gingiva.  The  alveolar  process  for  a  short  distance  beyond  the 
crest  was  also  absent. 

ing,  the  peridental  membrane  and  alveolar  bone  eventually  be- 
come involved.  The  foregoing  description  applies  to  a  group  of 
cases  in  which  treatment  by  instrumentation  is  of  only  temporary 
value  unless  it  is  carried    out    at    frequent    enough    intervals    to 


490  DENTAL   PATHOLOGY 

prevent  the  recurring  infection  from  acquiring  an  impregnable 
foothold  on  the  tissues. 

The  systemic  factor  is  frequently  associated,  in  etiology,  with 
a  series  of  local  conditions,  the  same  as  are  responsible  for  the 
development  of  the  purely  local  forms  of  gingivitis  and  pyorrhea — 
which  leads  to  equivocal  conclusions.  Under  those  circum- 
stances frequently  the  local  causes  alone  are  incriminated,  when 
as  a  matter  of  fact  the  systemic  disorder  is  frequently  just  as 
much  at  fault.  The  former  set  of  causes  incite  the  disease,  the 
latter  perpetuate  it. 


1  i 

■-, 

-V.V 

■ 

•  -JF         !*c 

'. :% 

' 

JUL.* 

J^i        '      ji        I 

# 

V 

p;~ 

V 

c 

>' ' « 

Fig.  401. — Destruction  of  alveolar  process  in  an  extensive  case  of  pyorrhea  alveolaris. 
Specimen  was  secured  from  Anatomical  Laboratories  of  the  College  of  Dentistry,  L  ni- 
versity  of   Southern   California,   and   photographed   by   Dr.   A.    C.    La   Touche. 

In  another  group  of  cases  local  causes  are  apparently  absent, 
or  if  present  are  not  possible  of  determination  unless  the  operator 
carry  out  a  very  minute  examination  of  the  gingival  tissues.  The 
infection  in  these  apparently  obscure  cases  frequently  originates 
in  the  subgingival  cul-de-sac  (subgingival  trough),  and  the  initial 
irritation  is  traceable  to  the  decomposition  by  putrefaction,  fer- 
mentation, or  both,  of  the  slimy  deposits  in  proximity  to  the 
gingival  structures.  These  slimy  deposits  are  particularly  evi- 
dent in  badly  neglected  mouths  and  in  those  of  people  who  neg- 


PYORRHEA     \l-\  I  OLARIS  t!M 

lecl  the  toilel  of  their  teeth  immediately  after  meals.  These  de- 
bris c(msist  of  a  mixture  of  saliva  and  food  particles.  The  end 
products  of  this  decomposition,  whether  alkaline  or  acid,  irritate 
the  tissues  in  the  subgingival  trough,  and  infection  by  the  com- 
mon bacterial  inhabitants  of  the  mouth  soon  follows.  The  in- 
fection, once  becoming  established,  generally  persists,  notwith- 
standing the  mosl  careful  and  thorough  operative  and  therapeu- 
tic measures.  This  form  of  pyorrhea  alveolaris  originates  and 
persists  independent  of  calcareous  deposits.  Some  investigators 
—the  late  G.  V.  Black  in  particular — incline  strongly  toward 
the  elimination  of  the  systemic  factor,  attributing  to  purely  local 
causes  all  the  phases  and  characteristics  of  the  disease.  That  a 
considerable  proportion  of  cases  is  of  local  causation  is  admitted 
by  practically  all  investigators,  hut  that  all  cases  are  of  that 
origin  has  not  received,  happily,  that  unanimous  acceptance. 

The  evidence  of  clinical  observation  strongly  points  to  many 
systemic  disturbances  as  etiologic  factors  in  pyorrhea  alveolaris. 
Certain  forms  manifest  themselves  as.  complications  of  digestive, 
renal,  or  pulmonary  disturbances;  and  again,  a  form  of  loosening 
of  the  teeth  is  the  result  of  a  gradual  and  progressive  atrophy  of 
the  investing'  structures  of  the  tooth,  occurring  in  connection 
with  arteriosclerosis,  atheroma,  anemia,  etc.  In  the  case  of  the 
latter  group  of  diseases  the  loss  of  the  teeth  is  the  result  of  true 
atrophy  of  the  peridental  membrane  and  alveolar  process,  due  to 
the  fact  that  the  gingiva,  peridental  membrane  and  alveolar  proc- 
ess, being  end-organs  as  previously  stated,  have  their  nutrition 
greatly  impaired  by  abnormal  changes  in  the  circulatory  appara- 
tus. These  dental  manifestations  become  evident  even  before  they 
induce  manifestations  of  a  more  serious  nature  in  any  of  the  vital 
organs. 

Miller,  as  far  back  as  1885,  submitted  a  series  of  investigations 
concerning  the  bacteriology  of  pyorrhea  alveolaris,  and  came  to 
the  conclusion,  which  holds  true  today,  that  pyorrhea  alveolaris 
is  not  caused  by  any  specific  bacterium,  but  is  highly  polymicro- 
bic in  character.  Various  bacteria  are  concerned  in  the  process, 
just  as  is  the  case  with  suppurations,  in  which  not  only  one,  but 
various  species  of  bacteria  are  active.  The  following  is  an  ex- 
cerpt of  Miller's  investigations: 


492  DENTAL   PATHOLOGY 

"When  the  disease  is  so  far  advanced  as  to  necessitate  the  ex- 
traction of  teeth,  Ave  first  cleanse  the  crown  and  neck  of  the 
tooth,  as  well  as  the  adjacent  gums,  with  5  per  cent  carbolic  acid  ; 
and  then,  after  removing  the  antiseptic  with  sterilized  cotton 
carefully  extract  the  tooth  so  as  not  to  graze  the  gums,  cheek 
or  lips  with  the  apex  of  the  root.  A  small  quantity  of  pure, 
fresh  pus  will  be  found  on  the  root  at  the  border  between  the 
dead  and  the  living  pericementum.  I  used  this  matter,  as  well 
as  part  of  the  periosteum  of  the  apex  of  the  root,  in  my  culture 
experiments.  In  order  to  obtain  in  pure  culture  the  bacteria  pos- 
sibly contained  in  the  cement-corpuscles  or  dentinal  tubules,  I 
placed  the  tooth  for  a  short  time  in  a  sublimate  solution  of  1  :;")000 
(so  as  to  destroy  the  £>'erms  on  the  surface).  Thereupon  it  was 
rinsed  in  a  large  quantity  of  sterilized  water,  dried  with  steri- 
lized blotting-paper,  and  the  outer  layers  removed  with  a  steri- 
lized knife.  Small  particles  from  the  deeper  layers  were  then 
scattered  on  a  culture  plate.  If  extraction  is  not  desirable,  we 
may  proceed  in  the  following  manner:  The  neck  of  the  tooth  is 
carefully  cleansed  and  a  slight  pressure  exerted  on  the  gums;  by 
this  means  the  desired  pus  is  pressed  out  between  the  sums  and 
the  neck  of  the  tooth. 

"I  made  dilution  and  line-cultures  on  beef -water  peptone 
gelatin  of  twenty-seven  teeth  afflicted  with  pyorrhea  alveolaris. 
The  gelatin  was  liquefied  in  five  cases  only.  Staphylococcus 
pyogenes  aureus  developed  but  once;  likewise  Staphylococcus  pyo- 
genes albus. 

"Two  formed  yellow,  one  green  coloring-matter:  the  latter  is 
of  interest  from  the  fact  that  it  forms  no  pigment  when  the  access 
of  air  is  prevented;  if.  however,  the  liquefied  colorless  gelatin 
is  shaken  with  air,  a  beautiful  deep  green  color  almost  imme- 
diately forms.  In  most  cases  I  obtained  but  one  kind,  or  one  kind 
so  predominated  that  the  rest  could  be  left  out  of  account.  In 
Cases  8  and  13  the  bacteria  cultivated  were  found  to  be  identical; 
also  in  Cases  lfi  and  17.  In  all  the  rest  they  were  different;  that 
is  to  say,  twenty-seven  cases  yielded  twenty-two  different  kinds 
of  bacteria. 

"From  these  experiments  Ave  might  conclude  that  if  there  is 
a  specific  bacterium  of  pyorrhea  alveolaris,  it  does  not  readily 
sjroAv  on  gelatin,  a  result  which  is  of  value  in  so  far  as  it  indicates 


PYORRHEA    ALVEOLARIS  193 

that  in  further  experiments  on  this  subjed  media  should  be  em- 
ployed which  admit  of  being  kept  at  the  temperature  of  the 
mouth.  At  the  same  time  the  thoughl  suggests  itself  that  possi- 
bly tlic  bacterium  of  pyorrhea  alveolaris,  like  so  many  mouth  bac- 
teria, is  cultivated  on  mine  of  the  artificial  nutrient  media,  which 
would  of  course  render  all  experimenting  useless. 

"The  few  experiments  which  were  made  on  animals  resulted 
negatively.  The  gums  of  healthy  dogs  (these  animals  often  suf- 
fer from  pyorrhea  alveolaris)  were  slightly  detached  from  the 
neck  of  the  tooth  and  inoculated  with  pus,  as  well  as  with  the 
deposits  on  teeth  attacked  by  the  disease.  Slight  inflammation 
invariably  ensued,  in  one  ease  also  a  little  suppuration,  hut  in- 
side of  a  week  all  eases  were  completely  healed.  Further  experi- 
ments are  necessary  to  determine  whether  positive  results  may 
be  gained  in  the  ease  of  old  or  emaciated  and  sick  dogs. 

"I  next  made  a  series  of  culture  experiments  on  agar-agar,  at 
blood  temperature.  Twelve  eases  of  pyorrhea  in  human  beings 
and  six  in  dogs  wi^v  examined.  I  isolated  twenty  different  bac- 
teria from  human  beings  and  nine  from  dogs.  Among  the  twenty 
kinds.  Staphylococcus  pyogenes  aureus  Avas  found  twice.  Staphy- 
lococcus pyogenes  albus  once.  Streptococcus  pyogenes  once.  Of 
the  other  sixteen,  nine  subcutaneously  injected  produced  no  particu- 
lar reaction,  four  a  slight,  and  three  a  severe  suppuration  in  the 
subcutaneous  connective  tissue. 

"Among  the  nine  species  in  dogs,  Staphylococcus  pyogenes  al- 
bus occurred  once.  Of  the  other  eight,  two  subcutaneously  in- 
jected caused  no  reaction,  five  but  a  slight,  and  one  very  profuse 
suppuration,  by  which  large  portions  of  skin  were  thrown  off. 

"I  succeeded,  consequently,  in  cultivating  a  large  number  of 
bacteria  of  pyorrhea  alveolaris  which  possessed  pyogenic  proper- 
ties, but  was  not  able  to  determine  the  constant  occurrence  of  any 
particular  one  which  might  be  defined  as  the  specific  microorgan- 
ism of  pyorrhea  alveolaris. 

"The  microscopical  examination  of  stained  sections  revealed 
masses  cf  different  bacteria,  cocci  and  bacilli,  and  more  seldom 
leptothrix.  on  the  surface  of  the  cementum.  and  where  there  were 
microscopic  cavities  in  the  cementum.  or  the  dentinal  tubules  were 
exposed  in  consequence  of  resorption,  the  microorganisms  Avere 
found  to  have  penetrated  for  a  short  distance." 


494 


DENTAL    PATHOLOGY 


M.  T.  Barrett  in  collaboration  with  Dr.  Allen  J.  Smith5,  in  an 
examination  of  forty-six  patients,  found  endameba  buecalis  in 
the  contents  of  pyorrhea  pockets,  and  the  absence  of  endameba  in 
seven  patients  with  no  recognizable  lesion  of  the  peridental  mem- 
brane. These  findings  were  taken  up  by  a  large  number  of  men 
in  the  medical  and  dental  professions  as  satisfactory  evidence  of 
the  pathogenic  importance  of  this  parasite  in  pyorrhea  alveola ris. 
That  such  a  conclusion  was  unwarranted  by  the  findings  of  Bar- 
rett, Allen  J.  Smith,  Bass,  and  Johns  is  now  a  generally  admitted 
fact.  Chiavaro6,  among  others  has  concluded  that  the  endameba 
buecalis,  while  it  is  found  in  the  pus  of  pyorrhea  alveolaris,  has 
not  a  pathogenic  action:  but  to  the  contrary,  as  it  feeds  on  bac- 
teria, "it  is  most  probably  an  aid  to  the  auto  disinfection  of  the 
mouth. ' ' 

A  study  of  cultures  from  pyorrhea  pockets  of  forty-seven  pa- 
tients by  J.  Marion  Read  gives  the  results  shown  in  the  accom- 
panying table  : 


ORGANISM 

1.  Staphylococcus  pyogenes  albus 

2.  Streptococcus   pyogenes 

3.  Pneumocoeeus 

4.  Micrococcus  eatarrhalis 

5.  Diplococcus  mucosus 

6.  streptococcus    viridans 

7.  Staphylococcus   aureus 
S.  Bacillus   mucosus 

9.  Friedlander  's  bacillus 

10.  Streptococcus   mucosus 

11.  Bacillus  proteus 

12.  Streptococcus    (in   short    chains) 

13.  Bacillus  coli 

11.  Bacillus   prodigiosus 

15.  Diphtheroid  bacillus 

16.  Bacillus  pyocyaueus 


ALONE 

ONE 

TWO 

TOTA 

OTHER 

OTHERS 

1 

10 

18 

29 

1 

G 

11 

18 

2 

12 

14 

3 

6 

9 

1 

4 

8 

3 

3 

1 

7 

4 

o 

6 

2 

4 

6 

2 

2 

4 

1 

2 

3 

2 

2 

2 

2 

1 

1 

1 

1 

1 
1 

1 
1 

EBarrett   and    Smith:      Dental   Cosmos,    1914. 
cChiavaro:     Dental   Review. 


CHAPTEE  XXXVIII 

PYORRHEA  ALVEOLARIS  AND  PERICEMENTAL 

ABSCESS  OF  GOUTY  ORIGIN* 

With  diseases  of  suboxiclation  characterized  by  the  presence  of 
given  amounts  of  urates  of  sodium,  calcium,  magnesium  and  am- 
monium in  the  blood,  the  presence  of  inflammatory  disturbances 
in  the  investing  tissues  of  the  teeth  has  been  associated. 

The  "gouty  diathesis,"  or  as  it  is  better  described  by  French 
writers,  the  diathesis  of  arthritism,  is  a  condition  characterized 
by  the  presence  in  the  blood  and  tissues  of  an  excess  of  the  prod- 
ucts of  the  incomplete  oxidation  of  protein  bodies  in  the  shape 
of  xanthin  bases,  amido  acid  compounds,  and  uric  acids.  The  dep- 
osition of  uratic  salts  upon  the  roots  of  teeth  seems  to  occur  in 
that  diathetic  state.  Urates  are  held  in  solution  in  the  blood  by 
virtue  of  the  alkalinity  of  that  fluid,  so  that  when  the  blood 
passes  over  an  area  of  decreased  alkalinity  or  of  actual  acidity, 
the  urates  are  precipitated.  These  uratic  deposits  are  the  source 
of  a.  degree  of  irritation  to  the  peridental  membrane  which  re- 
suits  in  the  establishment  of  areas  of  decreased  resistance — a 
'locus  minoris  rcsistcntux — in  which  bacteria  thrive  successfully. 
The  area  of  decreased  resistance  becomes  infected  by  bacteria,  and 
suppuration  follows.  Pus  is  of  a  degree  of  alkalinity  greater 
than  that  of  the  blood,  which  fact  accounts,  according  to  Kirk, 
for  the  precipitation  of  calcium  salts  upon  and  around  a  nucleus 
of  uratic  deposits.  The  discharge  from  this  area  of  infection  may 
take  place  along  the  gingival  margin,  this,  of  course,  occurring  af- 
ter the  infection  has  destroyed  an  area  of  tissue  extending  from 
the  primary  seat  of  the  infection  to  the  gum  margin. 

The  etiology  of  pericemental  abscess — an  abscess  upon  an  area 
of  the  peridental  membrane  of  a  tooth  containing  a  live  pulp 
and  supported  by  investing  tissue  whose  continuity  at  the  neck  of 
the  tooth  is  unbroken — is  fundamentally  alike  to  that  of  pyorrhea 
alveolaris  of  systemic  origin,  associated  with  the  uric  acid  diathe- 
sis. This  difference,  however,  exists:  that  in  pericemental  abscess 
the  pus  discharges  into  the  mouth  from  an  opening  in  the  gum 

*Kirk,  E.  C. :  Abscesses  upon  Teeth  with  Living  Pulps,  Dental  Cosmos,  1898.  Peri- 
cemental Abscesses,  Dental  Cosmos,  1900. 

493 


496  DENTAL    PATHOLOGY 

tissues  opposite  the  area  of  infection;  whereas,  in  pyorrhea  al- 
veolaris the  discharge  is  at  tlie  margin  of  the  gum.  Any  abscess 
which  originates  from  an  infection  of  the  peridental  membrane 
secondary  to  suppuration  and  putrefaction  of  the  pulp,  and  which 
discharges  into  the  mouth  through  a  sinus,  is  not  a  pericemental 
abscess.  \'>y  pericemental  abscess  is  definitely  understood  that 
it  is  ;i  condition  in  which  an  abscess  develops  upon  -ome  aspect 
of  the  peridental  membrane  of  a  tooth  having  a  live  pulp.  Peri- 
cemental abscesses  may  be  subpericemental  or  intrapericemental. 
according  to  whether  the  destruction  of  tissue  by  bacteria  has 
taken  place  under  the  pericemental  membrane,  bulging  it  out, 
and  eventually  rupturing  it.  or  within  the  fibrous  substance  of 
the  peridental  membrane1. 

Etiology  and  Pathologic  Anatomy  of  Pyorrhea  Alveolaris  and 
Pericemental  Abscess  of  Gouty  Origin 

It  is  a  well  known  fact  thai  the  salts  of  uric  acid  arc  maintained 
in  solution  in  the  blood  by  virtue  of  the  alkalinity  of  that  fluid 
and  that  they  are  precipitated  by  acids,  or  at  leasl  by  substances 
of  a  lower  degree  of  alkalinity  than  thai  of  the  solvenl  in  which 
tiny  are  present.  Scheele,  as  early  as  177*1.  had  discovered  the 
fact  that  urinary  concretions  are  dissolved  by  alkalies,  and  pre- 
cipitated by  acids.  The  application  of  these  known  facts  to  the 
conditions  present  in  the  peridental  membrane  can  be  made  to 
explain  the  phenomenon  of  the  formation  of  uratic  deposits  upon 
the  roots  of  teeth. 

If,  as  has  been  previously  pointed  out,  and  as  does  occur, 
uratic  salts  are  precipitated  by  preference  ;)t  -ome  point  in  tin- 
apical  region  of  the  tooth  root,  it  necessarily  follows  that  there 
the  fluids  and  structures  musl  be  of  a  degree  of  alkalinity  less 
than  that  of  the  blood.  Several  years  ago,  in  the  course  of  a  de- 
tailed study  of  pyorrhea  alveolaris  of  gouty  origin,  this  phase  of 
etiology  was  forcefully  brought  to  the  author's  attention  by 
reason  of  a  conspicuous  lack  of  reference  in  our  literature  to  this 
initial  phenomenon  in  the  evolution  of  thai  form  of  pyorrhea. 

Ordinarily,  that  is  to  say.  under  conditions  of  rest  or  slight 
activity,  all  articulations,  their  ligaments,  synovial  membranes, 
articulating  cartilages,  and  the  fluids  in  which  they  are  bathed, 

'Kirk,   E.   C:     Pericemental   Aliscess,   Dental  Cosmos, 


PYORRHEA    \l.\  lol.AUIs  4!»< 

are  of  an  alkaline  reaction;  on  the  other  hand,  under  conditions 
of  activity  the  reaction  a1  once  changes  to  one  of  less  alkalinity 
(relative  acidity),  or,  in  extreme  cases,  to  one  of  actual  acidity. 

These  reactions  of  the  tissues  in  question  constitute  a  physiologic 
fact  which  is  frequently  demonstrated  to  students  in  medical  and 
dental  schools  in  the  course  of  their  studies  of  general  physi- 
ology, and  requires  no  argument  to  substantiate  its  trustworthi- 
ness. A  comparatively  simple  experiment  will  convince  one  that 
the  reactions  are  as  here  stated.  After  preparing  a  frog  for  ex- 
perimentation by  first  severing  the  spinal  cord  at  its  .junction 
with  the  encephalon,  expose  the  middle  articulation  of  either  of 
the  hind  le^s  and  test  the  reaction  with  litmus  paper.  It  will  he 
found  decidedly  alkaline.  Xow  suhject  the  exposed  tissues  to  a 
series  of  active  contractions  through  electrical  stimulation,  and 
again  test  their  reaction.    It  will  be  found  to  be  markedly  acid. 

These  changes  in  reaction,  no  doubt,  also  occur  in  the  ease  of 
the  alveolodental  articulation.  The  peridental  membrane  is  com- 
posed of  bundles  of  fibrous  connective  tissues  which,  upon  being 
subjected  to  abnormal  degrees  of  irritation,  undergo  a  chemical 
disintegration  ending,  it  is  believed,  in  the  production  of  acid 
compounds.  Collagen,  the  principal  element  in  fibrous  tissue. 
when  hydrated  is  converted  into  gelatin  which,  upon  further  dis- 
integration, is  found  to  be  composed  of  proteins;  these  may  be 
detected  by  any  one  of  the  known  proteic  reactions.  Proteins. 
upon  breaking  down  during  activity,  may  give  rise  to  sarcolac- 
tic  or  the  plain  lactic  acid,  among  other  compounds.  It  is  submit- 
ted that  the  above  facts  satisfactorily  explain  the  conditions 
which  take  place  in  the  apical  region  of  the  root,  and  which,  in 
the  presence  of  pus-producing  organisms,  lead  to  the  development 
of  a  tophus  abscess.  As  an  additional  argument  of  the  theory 
under  consideration,  it  may  be  stated  that  the  frequency  of  gouty 
deposits  upon  the  metatarso-phalangeal  articulation  of  the  greal 
toe  is,  in  the  writer's  opinion,  due  to  the  fact  that  in  tin1  act  of  walk- 
ing a  great  proportion  of  the  body's  weight  is  thrown  upon  that 
part  of  the  foot.  The  consequence  of  this  strain  results  in  the 
formation  of  acid  substances,  and  so  renders  that  particular  re- 
gion a  suitable  field  for  the  precipitation  of  uratic  salts. 

It  will  he  seen,  therefore,  that  the  initial  phenomenon  re- 
sponsible for  the  deposition  of  uratic  salts  in  any  articulation   is 


498  DENTAL    PATHOL' 

the  result  of  a  change  in  the  reaction  of  the  tissues  brought 
at  by  the  breaking  down  of  protein  bodies  in  the  course  of 
physical  activity,  and  the  consequent  formation  of  acid  sub- 
stances. In  the  case  of  the  alveolodental  articulation,  -whenever 
-  ibjected  to  a  .  ■  of  activity  greater  than  normal. 
the  eatabolism  of  the  cellular  elements  of  the  peridental  mem- 
brane results  in  the  production  of  acid  substances  which  les 
the  alkalinity  of  the  membrane,  particularly  at  the  point  at 
which  the  greatest  degree  of  stress  is  felt.  In  single-rooted  teeth 
the  uratic  deposits  are  found  as  a  rule  in  or  near  the  apical  re- 
gion of  the  root,  and  in  multirooted  teeth  either  upon  one  of 

ts  in  a  location  c  .ding  to  that  upon  which  the  uratic 

salts  are  deposited  in  incisors,  canines,  and  bicuspids,  or  else  upon 
the  bifurcation  area.  These  areas  of  uratic  precipitation  are  ac- 
counted for  by  the  fact  that  in  the  pri  E  the  slightest  degree 
of  overactivity  the  loea*:  -  -rred  to  are  the  ones  which  sus- 
tain the  greatest  degree  of  stress,  for  reas  a  slusively  physical 
and  based  upon  laws  of  mechanics.  Teeth  re  very  often,  in  fact 
more  often  than  is  generally  believed,  subjected  to  degrees  of  sfa  ss 
greater  than  normal. 

A  slight  deviation  from  the  position  which  a  given  tooth  should 
occupy  in  the  arch  is  sufficient  to  cause  that  tooth  to  perform 
an  amount  of  -  greater  than  its  normal  share   should  be. 

This  leads   I        .eraetivity.   e  delation,   decrease   of  al- 

kalinity, and  probably  to  the  formation  of  lactic  acid  through  the 
breaking  down  of  the  complex  protein  molecules  of  the  peridental 
membrane,  and  finally  to  the  precipitation  upon  the  areas  under 
greater  stress  of  the  uratic  salts  held  in  solution  in  the  blood  by 
virtue  of  its  alkalinity. 

In  a  large  number  of  instances  of  pyorrhea  alveolaris.  or  peri- 
cemental al  >s  _  igin,  the  main  et:  _  causative 
factor  is  the  relative  or  actual  acidity  of  some  portion  of  the  peri- 
dental membrane.  This  is  then  followed  by  the  precipitation  of 
uric  acid  salts  which,  acting  as  an  irritant,  convert  that  peridental 
area  into  a  suitable  field  for  the  development  of  pyogenic  organ- 
isms. The  deposited  urates  create  a  locus  minoris  resistentia?.  and 
the  pyogenic  organisms  which  find  there  a  suitable  field  for  devel- 
opment are  responsible  for  the  formation  of  pus,  which,  beinsr 
of  an  alkalinity  greater  than  that  of  the  blood,  causes  a  precipi- 


PYORRHEA    A.LVEOLARIS  499 

tation  of  the  calcium  phosphates  thai  are  frequently  found  to  be 
componenl  of  the  gouty  deposit  (Kirk).  As  the  result  of  the 
infectious  process  which  spreads  by  continuity  to  the  alveolar 
process  and  gum  tissue,  a  sinus  is  established.  If  the  sinus  should 
lead  directly  to  and  through  the  gum,  a  pericemental  abscess  will 
be  established;  if  the  infection  and  consequent  tissue  destruction 
should  involve  the  peridental  membrane  and  alveolar  process 
along  the  side  of  the  root  to  the  neck  of  the  tooth  a  so-called 
pyorrhea  pocket  will  result. 


CHAPTER  XXXIX 

THE  DENTAL  PULP  AXD  ITS  DISEASES 

The  dental  pulp  is  the  soft  tissue  contents  of  the  pulp  chamber 
and  root  canals  of  teeth  (Figs.  402  and  403).  It  is  in  close  relation 
with  the  peridental  membrane  at  the  apical  foramen  (Fig.  404). 
It  is  the  remains  of  the  dental  papilla — the  aggregation  of  connec- 
tive-tissue cells — supported  by  a  framework  of  minute  fihrilhe. 
It  presides  over  the  formation  of  dentin  during  the  developmental 
period  of  the  tooth  and  throughout  the  life  of  the  tooth  in  response 
to  physiologic  and  pathologic  stimuli.  It  occupies  the  pulp 
chamber  in  the  crown  of  the  tooth  and  the  root  canal  or  canals 
in  the  root  of  the  tooth.  Its  outline  is  in  a  general  way  thai  of 
the  tooth  in  which  it  is  contained.  It  resembles  embryonic  tissue  in 
its  delicate  fibrillar  basis,  and  in  its  cells  which  are  round,  oval  or 
stellate.  The  dental  pulp  is  proportionately  larger  the  younger 
the  individual,  and  becomes  smaller  with  aye  as  the  hulk  of  dentin 
increases.  It  is  the  sensory  organ  of  the  tooth  and  the  source  of 
the  blood  and  nerve  supply  of  the  dentin.  After  the  dentin  at- 
tains its  full  development,  the  pulp  deposits  new  dentin,  through 
the  agency  of  its  odontoblasts,  under  conditions  of  abnormal 
stimulation  and  as  a   physiologic  manifestation  of  increasing  age. 

Histologic  Constituents 

The  histologic  constituents  of  the  dental  pulp  are  six,  to  wit: 

1.  Odontoblasts. 

2.  Layer  of  Weil. 

3.  Connective-tissue  cells. 

4.  Intercellular   substance. 

5.  Blood  vessels. 

6.  Nerves. 

Odontoblasts. — Odontoblasts  are  tall,  columnar  cells  lining  the 
pulp  on  the  dentin  side  (Fig.  405).  They  are  about  twenty-five 
microns  in  length  and  five  in  width.  The  nucleus  is  located  to- 
ward the  pulpal  side,  viz.,  away  from  the  dentin  wall.  They 
form  a  protecting  layer  around  the  pulp,  and  from  the  fact  that 

500 


THE    DENTAL    PULP    A.ND    [TS    DIS1   v-i  S 


501 


Vie  40'— A  longitudinal  section  of  a  normal  pulp  of  man.  a.  a.  a.  a  odontoblastic 
layer-  &  nerve  trunk;  c,  c,  plexus  of  nerves  under  odontoblastic  layer.  The  connective 
?«ue  cells  distributed  everywhere  in  the  matrix  of  the  pulp  are  of  three  kinds,  round, 
spfndleshape  and  stellate.      The   latter   are   fewer  in   number   and   more   difficult   to   locate. 


502 


DENTAL    PATHOLOGY 


they  adhere  to  the  walls  of  the  root  canals  they  have  been 
collectively  named  the  menibrana  eboris.  The  odontoblastic 
layer  of  the  pulp  is  the  only  connective  tissue  in  the  body 
having  cells  of  columnar  form.  This  columnar  form  does  not, 
however,  persist  throughout  the  life  of  the  pulp.  It  is  particu- 
larly evident  prior  to  and  during'  the  formation  of  dentin;  but 
in  old  pulps,  i.  e.,  after  dentin  has  been  formed,  the  odontoblasts 
are  round  or  oval.  They  are  the  specific  dentin-produeing 
cells — a  function  which  they  retain  throughout  the  life  of  the 
pulp.     They  send  processes  into  the  tubules  of  the  dentin — the 


Fig.   403. — Longitudinal   section  of  normal   pulp.     The   same   structural   elements  are   to   be 
found   as   are  indicated   in   the   previous   section. 


dentinal  fibrillar  or  fibers  of  Tomes,  and  probably  are  connected 
among  themselves  by  delicate  fibrous  processes. 

Layer  of  Weil. — The  layer  of  "Weil  is  supposed  to  be  that  por- 
tion of  the  pulp  lying  between  the  odontoblastic  layer  on  the 
outside,  and  the  portion  of  the  pulp  which  is  thickly  studded 
with  connective-tissue  cells  distributed  throughout  the  gelati- 
nous matrix  of  the  pulp  on  the  inside.  It  itself  is  described  as 
being  very  sparingly  embedded  with  connective-tissue  cells.  In 
numerous  specimens  this  layer  does  not  exist,  but  whether  pres- 


THE    DENTAL    ITU'    AND    ITS    DISEASES 


503 


ciil  or  not,  is  of  qo  physiologic  import.  Von  Ebner  has  attributed 
the  layer  of  Weil  to  shrinkage  of  the  body  of  the  pulp,  while 
WahlkoflE  considers  thai  the  phenomenon  is  caused  by  a  shrink- 
age of  the  odontoblasts.  11  is  best  studied  in  transverse  sections. 
Connective-tissue  Cells. — The  connective-tissue  cells  of  the  pulp 
are  of  three  shapes — round,  spindle-shaped  and  stellate.     In  Fig. 

Apical   foramen 


[i  ntal 
membrane .  . 


I  it  -mm  . 


V 


Dentin 


.  .  Bone  of  alveolar  process 


.  Peridental   membrane 


.  Dentin 


.  Dentin 


Pulp 

Fig.  404. — Section  of  a  tooth  showing  relation  of  the  pulp  at  the  apical  foramen  to  the 
peridental  membrane.  Some  of  the  blood-vessels  are  shown  partly  filled  with  blood  cells. 
The  fibrillar  character  of  the  pulp  matrix  is  seen. 


402  the  round  and  spindle-shaped  cells  are  readily  distinguished, 
but  the  stellate  cell  is  very  rare  and  exceedingly  difficult  to  find, 
being  best  shown  by  focusing  for  depth. 

Intercellular  Substance. — The  intercellular  substance  is  a  gelat- 
inous mass  resembling  the  tissue  found  in  the  umbilical  cord, 
and  known  as  Wharton's  jelly.     It  is  an  immature  form  of  con- 


504  DENTAL    PATHOLOGY 

nective-tissue  consisting  of  very  fine  fibrillae.  Besides  these  ex- 
tremely slender  fibrous  elements,  connective-tissue  fibers  of  or- 
dinary size  are  also  found  supporting  the  blood  vessels  and 
nerves. 

Blood  Vessels. — The  pulp  has.  relatively  speaking,  a  very  rich 
blood  supply.  During  the  formative  period  of  the  tooth  the 
blood  is  carried  to  it  by  means  of  several  arteries.  "When  the 
development  of  the  tooth  is  completed  the  blood  supply  consists 
as  a  rule  of  one  small  artery  and  a  correspondingly  small  vein, 
or  again  the  arrangement  may  consist  of  three  or  more  arteries 
with  their  corresponding  thin-walled  veins  entering  the  tooth 
through  one  or  several  foramina.  Weil  has  found  that  from 
three  to  ten  blood  vessels  may  enter  the  tooth  through  the  apical 
foramen.  The  difficulties  attending  the  treatment  of  roots  pos- 
sessed of  more  than  one  apical  foramen  are  obvious.  This  artery, 
or  arteries,  breaks  up  into  numerous  branches  which  are  distrib- 
uted throughout  the  substance  of  the  pulp,  and  as  these  branches 
reach  the  odontoblastic  layer  they  split  into  capillary  plexuses, 
which  lie  in  close  proximity  to  the  odontoblastic  cells,  from  where 
veins  carry  off  the  venous  blood.  The  walls  of  the  vessels  of  the 
pulp  are  very  thin  and  easily  affected  by  changes  in  blood  pres- 
sure.1 

There  is  no  collateral  circulation  in  the  pulp,  so  that  any  in- 
jury to  the  blood  vessels  at  the  apex  affects  the  vitality  of  the 
entire  pulp.  As  shown  by  A.  Hopewell-Smith  its  veins  are  valve- 
less  and  noncollapsible.2 

Noyes  has  recently  demonstrated  that  lymphatics  exist  in  the 
pulp. 

Nerves  of  the  Pulp. — One  or  more  nerve  filaments  enter  the 
pulp  through  the  apical  foramen,  each  filament  being  composed 
of  from  ten  to  thirty  medullated  nerve  fibers.  These  nerves 
enter  with  the  blood  vessels.  After  entering  the  pulp  tissues 
they  spread  out  into  plexuses  and  eventually  become  nonmedul- 
lated.  forming  rich  networks  close  to  the  odontoblasts.  The 
protoplasmic  prolongations  of  the  odontoblasts  are  the  only 
structures  which  have  thus  far  been  demonstrated  to  enter  the 
dentinal  tubuli,  and  until  such  time  as  nerve  fibrillse  can  be  dem- 


•Black,   G.   V.:     Dental  Pathology. 

2Hor>e\vell-Smith,    A.:      The    Histology    and    Patho-Histology    of    the    Teeth    and    Asso- 
ciated Parts,  Philadelphia,   P.   Blakiston's   Son  &  Co. 


0 


Fig.    405.- 


-Section  of  a  pulp  of  sheep,   showing  histologic   characteristics   of  odontoblastic 
layer.     Section  prepared  by  Dr.  A.  C.  La  Touche. 


THE    DENTAL    PULP    AM)    lis    DISEASES  -'^-> 

onstrated  within  the  tubules,  the  odontoblastic  prolongations  or 
fibers  of  'Pomes,  in usi  continue  to  be  looked  upon  as  the  only 
means  by  which  impulses  are  carried  from  the  dentin  to  the  pulp. 

Fibers  of  Tomes 

The  transmission  of  sensations  from  the  dentin  to  the  pulp 
lakes  place  through  the  medium  of  the  fibers  contained  in  the 
dentinal  tubuli.  These  fibers  are  prolongations  of  the  odonto- 
blasts and  while  physiologically  Ihey  play  the  role  of  nerves,  his- 
tologically they  in  no  way  resemble  nerve  tissue.  In  addition  to 
these  processes  of  the  odontoblasts,  a  process  arising  from  the 
pulp  end  of  the  odontoblasts,  and  a  process  on  eaeh  side  of  the 
cell  communicating  laterally  with  the  adjoining  odontoblasts. 
have  been  described.  These  additional  processes  are  not  dis- 
cernible  in  histologic  preparations  and  must  therefore  be  con- 
sidered for  the  present  at  least  in  the  light  of  histologic  specu- 
lations. 

Diseases  of  the  Pulp 

The  pulp,  because  of  the  character  of  its  blood  supply,  being 
devoid  of  collateral  sources  of  nutrition;  because  of  the  lack  of 
adaptability  of  its  vessels  to  changes  in  blood  pressure;  because 
of  the  character  of  its  immediate  surroundings,  hard  and  un- 
yielding; because  of  the  liability  of  its  protecting  tissues  (the 
enamel,  the  dentin,  and  the  cementum)  to  diseases  which  de- 
crease their  thickness  or  density,  and  hence  lessen  their  power 
to  act  as  barriers  against  disease-producing  influences,  thermal, 
chemical  and  bacterial, — is  susceptible  in  an  exaggerated  degree  to 
diseases  which  in  the  vast  majority  of  cases  impair  its  vitality 
permanently.  While  from  a  pathologic  standpoint  the  pulp  is 
subject  to  a  number  of  diseases,  each  of  which  will  be  discussed 
under  its  own  heading,  from  the  clinical  standpoint  diseases  of 
the  pulp  are  considered  from  two  main  aspects  only.  The  group 
in  which  conservative  measures  can  be  successfully  employed 
with  the  view  of  preserving  the  pulp,  is  one;  and  the  group  which 
demands  as  the  only  permanent  compromise  the  sacrifice  of  the 
organ,  is  the  other. 

In  the  first  group  is  included,  mainly,  hyperemia,  when  it  is 
a  pathologic  entity  in  itself  and  is  nonbacterial  in  origin.     In 


50G  DENTAL    PATHOLOGY 

the  second  group  are  included  all  diseases  of  bacterial  origin, 
and  those  persisted  forms  of  nonbacterial  hyperemia  which  lead 
to  nonseptic  pulpitis  and  death  of  the  organ. 

The  pulp  is  also  subject  to  retrograde  as  well  as  to  construc- 
tive metamorphoses.  In  the  former  group  are  included  the  fibroid 
degenerations  of  Eopewell-Smith,  and  those  presenting  similar 
characteristics  as  described  by  Talbot,  Latham,  Wedl,  Wahlkoff 
and  Rothman;  also  fatty,  hyaline  and  colloid  degenerations, 
recognized  only  upon  postmortem  examinations  of  the  pulp.' 

In  the  latter  group  are  included  calcareous  infiltration  of  the 
pulp,  calcifications  of  the  dentinal  tubuli,  pulp  nodules  and  secon- 
dary dentin. 

General  Predisposing  Causes 

In  the  discussion  of  diseases  of  the  pulp,  the  predisposing  as 
well  as  the  exciting  causes  should  be  considered.  The  predispos- 
ing causes  may  be  general  or  local.  Neither  heredity  nor  sex  are 
of  any  moment  in  this  connection.  Age  is  considered  as  a  pre- 
disposing cause  mainly  because  during  childhood  and.  say,  up 
to  sixteen  years,  children  do  not  take  care  of  their  teeth  in  a 
manner  conducive  to  the  prevention  of  caries,  and  consequently 
inflammation  of  the  pulp  is  more  frecpient  than  later  in  life, 
when  the  development  and  progress  of  caries  is  prevented  by 
hygienic  care  and  filling  operations.  As  the  child  grows  the  at- 
tacks of  toothache  from  pulpitis  and  pericementitis  become  les< 
frequent,  but  this  should  not  be  attributed  to  the  influence  of 
age  itself.  It  is  the  result  of  conditions  in  which  age  plays  no 
part  whatsoever.  Degenerations  of  the  pulp  are  more  frequent 
as  age  advances,  and  these  degenerations  "are  not  necessarily 
connected  with  the  actual  number  of  years  of  the  individual's 
life,  but  with  the  age  of  the  tooth  and  its  pulp."  Hopewell- 
Smith  has  found  evidence  of  retrograde  metamorphoses,  such  as 
fibroid  degenerations,  in  children's  deciduous  teeth,  identical  to 
Ihose  degenerations  incidental  to  old  age.4 

The  amount  and  the  composition  of  the  blood  varies  in  the 
presence  of  such  systemic  pathologic  states  as  affect  the  lungs, 
heart,  kidneys,  spleen,  pancreas,  stomach,  intestines,  the  blood, 
the  lymph,  the  nervous  system,  etc.,  and  these  abnormal  condi- 

sHopewell-Smith,    A.:      In    N.    G.    Bennett's    Science   and    Practice   of    Dental    Surgery, 
New   V..rk,  Win.   Wood  &  Co. 
iHopewell-Smith,   A.:     Ibid. 


THE    DENTAL    PULP    AND    ITS    DISEASES  501 

lions  doubtless  exerl  some  influence  upon  the  nutritional  proc- 
esses in  ilif  pulp.  The  same  must  be  s;ii<l  of  diseases  of  me- 
tabolism, which  become  in  time  the  precursors  of  chronic  dis- 
eases in  any  of  the  viscera,  and  which  leave  their  impress  upon 
the  pulp.  In  pyrexial  and  apyrexial  maladies,  degenerations 
(such  as  Patty  or  albuminous)  of  the  pulp  may  occur.5 

Anemia,  chlorosis  leukemia,  may  cause  cell  degenerations  in  the 
pulp.  Gout,  rheumatism,  and  allied  conditions  may  lead  to 
nodular  deposits  of  calcified  material  in  the  pulp.0 

Talbot's  investigations  go  to  show  that  changes  in  the  blood 
current  due  to  circulating  poisons  produce  a  deranged  metabo- 
lism in  the  pulp  which,  by  lowering  its  inherent  resistance,  ren- 
ders it  liable  to  any  of  the  several  pulp  diseases. 

Local  Predisposing  Causes 

Among  the  local  predisposing  causes  Hopewell-Smith  gives 
prominence  to  degenerative  changes  in  the  cells  of  the  pulp, 
broughl  ahout  by  insufficiency  of  arterial  blood  supply  and 
venous  drainage,  the  result  of  constriction  of  the  apical  foramen 
or  foramina.  After  the  age  of  twenty-five  he  has  found  that  a 
majority  of  teeth  have  apical  foramina  so  diminutive  that  they 
must  of  necessity  interfere  with  nutritional  changes  in  the  pulp 
and  lead  to  certain  types  of  degenerations.  It  is  unquestionable 
that  diminutiveness  of  apical  foramina  account  not  only  for  these 
degenerations,  but  also  for  the  fact  that  the  pulp  has  practically 
no  power  of  repair,  especially  as  the  age  of  the  tooth  increases. 

The  presence  of  metallic  and  of  nonmetallic  fillings  must 
also  be  considered  in  the  light  of  local  predisposing  causes, 
though  to  a  less  extent.  A  metallic  mass  in  the  tooth  may  lead 
to  calcific  degenerations  within  the  pulp,  these  foreign  calcified 
particles,  acting  as  sources  of  irritation  and  by  decreasing  the 
resistance  of  the  tissues,  favor  bacterial  invasion  from  the  ex- 
terior of  the  tooth,  or  via  the  blood  stream.  In  the  microscopic 
study  of  apparently  healthy  pulps  the  author  has  run  across 
specimens  showing  small  areas  of  chronic  inflammation  which 
must  have  existed  for  months,  or  perhaps  years.  The  bacteria 
were  evidently  overcome  to  the  extent  of  remaining  in  a  semi- 


5Hopewell-Smith,  A.:      Ibid, 

"Hopewell-Smith,  A.:     Ibid. 


508  DENTAL   PATHOLOGY 

quiescent  slate  for  sonic  lime,  causing  very  limited  tissue  de- 
struction and  eventually  their  replacement  by  cells  of  an  inferior 
organization. 

These  facts  arc  brought  out  to  overcome  the  prevailing  opinion 
that  the  pulp  lacks  in  toto  the  power  of  overcoming  infections, 
and  to  show  that  if  a  pulp  be  under  constant  stress  by  the  pres- 
ence of  calcific  liodies  within  its  substance,  such  a  power  of  re- 
sistance to  infection,  be  it  ever  so  small,  is  rendered  still  more 
insignificant,  or  is  completely  abolished.  Gysi  has  reported  the 
regeneration  (if  tissue  in  the  pulp  which  has  been  destroyed  by 
infection,  but  this  tendency  at  the  development  of  scar  tissue  in 
the  pulp  is  vevy  slight  and  rarely  encountered. 

Exciting  Causes:     General 

Again,  the  exciting  causes  may  be  general  or  local.  In  the 
general  are  included  changes  in  the  quantity  and  quality  of  the 
blood  as  the  result  of  chronic  intoxications  in  any  of  the  viscera, 
and  of  nervous  disorders.  These  changes  bring  about  cell  de- 
generations in  the  pulp,  which  gradually  impair  its  vitality  and 
shorten  its  period  of  physiologic  usefulness.  The  changes  in  the 
quantity  and  quality  of  the  blood  may  bring  about  diseases  of 
the  vessel  walls  and  changes  in  blood  pressure.  These  changes 
in  blood  pressure,  which  affect  the  arteries  throughout  the  body, 
must  necessarily  also  leave  their  impress  upon  the  vessels  of  the 
pulp.  It  is  thus  that  we  may  explain  the  pulp  hyperemia  which 
develops  in  the  course  of  febrile  disturbances.  The  congestion  of 
the  pulp  ceases  upon  the  elimination  of  the  causes  responsible 
for  the  general  rise  in  blood  pressure.  Here  are  instances  in  which 
nonbacterial  agencies  are  the  causative  factors  of  pulp  disease. 
Degenerations  of  the  pulp,  as  the  result  of  arteriosclerosis  fol- 
lowing typhoid  fever,  septicemia,  and  other  acute  infections,  have 
been  described  by  Talbot  who  has  also  observed  amyloid  and 
hyaline  degenerations  within  the  pulp. 

Neoplasm  of  the  pulp  has  been  described  by  Latham.7  It  oc- 
curred in  the  pulp  of  an  upper  cuspid  of  a  woman  aged  fifty-six 
giving  a  history  of  cancer  in  her  family.  Masses  of  cells  were 
observed  in  the  microscopical  sections  prepared  from  this  pulp, 
which  Latham  interpreted  as  carcinomatous. 

'Latham,   Vida   A.:     Neoplasm  of  the  Pulp,  Jour.  Am.  Med.  Assn.,  1904. 


THE   DENTAL    PULP   AND   ITS   DISEASES  509 

Exciting  Causes:     Local 

The  local  exciting  causes  are  dental  caries,  erosion,  abrasion, 
and  any  process  by  which  the  thickness  or  density  of  the  enamel, 
dentin  and  cementum  are  decreased.  In  caries  of  the  enamel, 
of  the  dentin,  and  of  the  cementum,  in  which  bacteria  have  not 
gained  access  to  the  pulp,  the  pathologic  manifestations  in  the 
pulp  are  the  result  mainly  of*  thermal  irritation,  although  chem- 
ical irritation  also  plays  a  part  in  the  process.  The  same  is  the 
case  with  erosion  and  abrasion.  The  degenerations  produced 
by  these  abnormal  stimuli  are  constructive  in  character  and  mani- 
fest themselves  in  overcalcification  of  the  dentinal  tubules,  cal- 
cific infiltrations  of  the  pulp,  and  the  formations  of  pulp  nodules. 
The  acid  end  products  of  carbohydrate  fermentation — the  acid 
concentration  being  increased  in  the  confines  of  the  cavity — is  a 
source  of  chemical  irritation  to  the  dental  pulp,  which  may  re- 
sult in  degrees  of  stimulation  leading  to  constructive  degenera- 
tions ;  or  when  of  greater  intensity,  to  pulp  inflammation  ending 
in  the  death  of  the  pulp.  Bacteria  which  invade  the  pulp  by  way 
of  a  carious  cavity  are  the  most  frequent  exciting  cause  of  inflam- 
matory disorders  of  the  pulp. 


CHAPTER  XL 

CALCIFIC  DEGENERATIONS  OF  THE  PULP  AND  OF  THE 
DENTINAL  TUBULI:     SECONDARY  DENTIN 

Whenever  the  protecting  tissues  of  the  pulp  suffer  a  decrease 
in  thickness  or  in  density  the  pulp  becomes  the  seat  of  nutri- 
tional changes.  The  reason  for  this  phenomenon  is  to  he  at- 
tributed  to  an  increase  in  the  intensity  of  thermal  stimuli.  The 
continued  action  of  these  abnormal  stimuli  results  in  an  over- 
activity of  the  odontoblasts,  or  denl  in-forming  cells.  The  odon- 
toblasts s<>  stimulated  deposit,  by  means  of  the  odontoblastic  pro- 
longations, inorganic  salts  in  the  dentinal  tubuli — tricalcium 
phosphate,  mainly.  The  anatomic  changes  "which  thus  result  are 
an  increase  in  the  density  and  in  the  thickness  of  the  walls  of 
the  tubuli,  and  possibly  a  decrease  in  the  size  of  the  dentinal 
fibrillar.  This  process  occurring  in  a  number  of  tubuli  results 
in  an  overcalcified  area,  the  transparent  zone  of  Tomes.  It  is 
the  result,  as  previously  stated,  of  odontoblastic  stimulation,  and 
is  brought  about  by  caries  of  the  enamel;  caries  of  the  dentin; 
erosion;  abrasion;  metallic  fillings;  involuntary  gritting  of  the 
teeth;  violent  brushing  of  the  teeth;  and  by  extremes  of  tem- 
perature, such  as  occur  during  a  meal.  Several  theories  have 
been  advanced  in  explanation  of  dentin  transparency,  or  the 
transparent  zone  of  Tomes.  Black1  attributes  this  phenomenon 
to  death  of  the  dentinal  fibrillar  in  the  transparent  zone  (hyaline 
zone)  from  the  irritation  caused  by  the  progress  of  caries.  John 
Tomes,  the  first  investigator  to  report  upon  dentin  transparency, 
attributed  it  to  a  calcification  of  the  dentinal  fibrillar,  or  an  in- 
filtration of  the  organic  filaments  by  calcium  salts.  We  consider 
it  as  the  expression  of  a  vital  process — in  fact  the  only  view 
tenable  today.  Miller's  experiments  must  be  accepted  as  final, 
or  at  least  so  until  such  time  as  the  weight  of  accumulated  evi- 
dence to  the  contrary  shall  be  forthcoming.  The  transparent 
zone  is  not  observable  in  pulpless  teeth,  unless  it  he  that  the 
phenomenon  occurred  prior  to  the  death  of  the  pulp  following 


1Black:     Operative   Dentistry,  Chicago,  Medico-Dental  Pub.   Co.,  i. 

510 


CALCIFIC    DEGENERATIONS  511 

infectious  processes  or  accidental  traumatisms,  but  occurs  in 
teeth  having  live  pulps  following  abnormal  degrees  of  irritation 
brought  about  by  the  scries  of  conditions  above  enumerated. 
Miller  has  reminded  us  thai  the  opacity  of  dentin  is  the  resull 
of  the  difference  in  indices  of  refraction  between  the  dentin  ma- 
trix (the  intertubular  substance ),  and  the  dentinal  tubules.  There 
are  two  ways  in  which  the  transparency  of  an  area  of  dentin  may 
be  brought  about.  In  the  one  ease  it  is  by  an  increase  in  the 
amount  of  calcified  substance  within  the  tubuli,  thus  equalizing 
(lie  coefficient  of  refraction  between  these  and  the  dentin  ma- 
trix; or  by  decalcification  of  t lie  dentin  matrix,  producing  the 
same  result.  That  decalcification  of  the  dentin  matrix  does  not 
occur  lias  been  shown  by  chemical  analysis;  and  as,  in  addition, 
a  diminution  in  the  caliber  of  the  tubuli  has  been  observed,  the 
conclusion  is  forced  upon  us  that  it  is  a  process  characteristic 
of  living  dentin  in  which  a  degree  of  transparency  is  attained 
by  the  increase  in  calcified  matter  in  the  tubuli,  which  to  some 
extent  equalizes  the  coefficients  of  refraction  of  these  and  the 
dentin  matrix.  Miller  observed  the  identical  phenomenon  in 
human  senile  teeth  in  which,  doubtless,  the  pulps  had  been  for 
many  years  subjected  to  mild  degrees  of  irritation,  in  roots  in 
the  process  of  resorption,  and  in  the  abraded  teeth  of  dogs. 

Secondary  Dentin 

There  occurs  either  in  conjunction  with  the  formation  of  the 
transparent  zone,  or  at  some  subsequent  time,  or  else  independent 
of  the  transparent  zone,  the  formation  of  additional  dentin  at 
the  expense  of  the  size  of  the  pulp  chamber  and  root  canals  (Figs. 
406-409).  The  secondary  dentin  so  formed  must  be  viewed  in 
the  light  of  a  stimulation  to  the  pulp  of  somewhat  greater  in- 
tensity than  that  which  follows  tubular  calcification.  Secondary 
dentin  is  classified  as  typical  or  amorphous,  the  typical  variety 
bein<i'  that  in  which  the  tubules  in  the  newly  formed  dentin  are 
more  or  less  evenly  distributed  and  resemble  normal  dentin.  The 
amorphous  is  that  in  which  the  secondary  calcification  does  not 
partake  of  the  character  of  primary,  normal  tubular  dentin.  The 
forms  of  amorphous  dentin  have  been  classified  by  Hopewell- 
Smith  as  areolar  dentin  containing  interglobular  spaces;  cellular 
dentin,   in  which  the  process  of  calcification  has   encapsulated 


512 


DENTAL   PATHOLOGY 


some  cells  of  the  pulp;  laminar,  in  which  laminated  masses  of 
calcific  mallei'  appear;  and  hyaline,  in  which  the  calcific  matter 


Fig.    406. — Secondary    dentin.      a,  a,    primary    dentin;    b,  b,    secondary    dentin;    c,  c,    pulp. 

has  a  smooth  appearance.  Secondary  dentin  may  also  occur 
through  reflex  action  by  reason  of  continued  irritation  in  ad- 
jacent teeth. 


c  OjCIFIC    DEGENER  \TK>\s 


513 


Fig.         407. — Secondary  Fig.         408. — Secondary 

dentin  which  entirely  filled  dentin  in  connection  with 
the  pulp  chamber,  the  abraded  upper  central, 
original  outlines  of  which 
can  be  distinguished  from 
the  secondary  formation. 
Abrasion  and  erosion  are 
responsible  for  the  vol- 
uminous depositions  of  sec- 
ondary dentin. 


Fig.  409. — Secondary 
dentin  in  connection  with 
severe   abrasion. 


Fig.  410. — Pulp  the  seat  of  a  chronic  inflammation,     a,  an  area  of  round-cell  infiltration. 


514 


DENTAL    PATIIOLOGV 


Pulp  Nodules 

Pulp  nodules,  or  pulp  stones,  are  amorphous  masses  of  calcific 
matter  found  in  the  pulp  chamber  or  in  the  root  canals.  It  is 
the  result  of  an  activity  of  the  pulp  caused  by  direct  or  indirecl 
abnormal  stimulations.  Pulp  nodules,  even  though  they  give 
rise  to  no  symptoms  whatsoever  during  their  deposition,  and 
sometimes  thereafter,  must  be  regarded  as  the  pathologic  mani- 


Fig.    411. — Chronic    inflammation    of    the   pulp.      The    degeneration    of    the    cells    and    fibers 
of  the   pulp   results   in   the   marked   areolation   seen   in   the   specimen. 


festations  of  disturbed  intrapulpal  metabolism.  The  pulp  nodule 
is  more  in  the  nature  of  a  secretion  within  the  pulp  of  the  sub- 
stances entering  into  the  composition  of  the  nodule.  In  at  least 
some  cases  it  follows  in  the  wake  of  chronic  inflammation  in 
limited  areas  of  the  pulp.  The  process  of  nodule  formation  is 
preceded  by  forms  of  cell  degenerations — hyaline   or  fatty.     In 


CALCIFIC    DEGENERATIONS 


515 


Fig.     412. — Pulp     stones     occupying    the  Fig-    413. — Pulp   stone    (nodule)    in   pulp 

entire   pulp   chamber.  chamber   of   lower   molar,      a.   Tooth   before 

splitting;   b,  and  c,  halves  of  the  tooth  with 
the   pulp   stone    in   situ. 


Fig.  414. — Pulp  nodule  filling  up  the 
entire  pulp  chamber.  The  nodule  is  not 
attached   to   the   walls   of  the  pulp   chamber. 


Fig.   415. — A  pulp   nodule   in   situ. 


51G 


DENTAL    PATHOLOGY 


_„_& 


Fig.    416. — Decalcified   section    with    pulp    stone    in   situ,      a,  a,    dentin;    b.  b,   pulp    stone    in 

situ;   c,   pulp. 


Fig.  417. — Decalcified  longitudinal  section,  showing  a  pulp  stone  in  place.  Notice 
the  onion  peel  arrangement  in  the  substance  of  the  stone.  It  is  not  attached  to  the 
walls  of  the  root  canal,     a,  a,  pulp;   b,  b,  dentin;   c,  c,  pulp  stone   in  situ. 


7  = 

ft 

i> 

3 -a 


■A*.,. 


wo 


ft 


,  t.  J.  -«... 


d:'"- 


CALCIFIC    DEGENERATIONS 


517 


pulps  studied  by  the  author  small  areas  of  chronic  inflammation 
have  been  found  which  bad  existed  probably  for  months  and 
years  without  giving  rise  to  any  symptoms  whatsoever  (Figs. 
410-411).  it  is  therefore  probable  thai  those  same  areas  become 
in  some  instances  pulp  nodules,  following  calcific  infiltration. 
Fatty  degeneration  is  responsible  for  the  liberation  of  fatty  acids 
which  at  first  combine  with  the  calcium  broughl  to  the  degenerat- 
ing cells  in  the  blood,  the  resulting  calcium — fatty  acid  compound 
being  decomposed  into  soluble  phosphate  or  carbonate  by  the  dis- 
placement of  the  fatty  acids  by  phosphoric  or  carbonic  acid. 
Pulp  nodules  do  not  resemble  dentin:  they  are  irregularly  shaped 
masses  ranging  from  such  a  size  as  to  be  visible  under  the  mi- 


*t 


Fig.    420. — Pulp   stones   in   pulp   chamber   of  upper  right  first  and   second   molars. 

croscope  only,  to  a  size  to  fill  up  the  entire  pulp  chamber  (Figs. 
412-420i.  The  teeth  in  which  pulp  nodules  exist  may  remain 
absolutely  quiet  and  comfortable,  and  again  may  give  rise  to 
severe  reflex  manifestations  in  the  shape  of  radiating  neuralgia, 
the  pain  traveling  in  the  direction  of  the  ear,  the  eye,  the  tem- 
ples, and  the  back  of  the  neck. 

Pulp  nodules  are  found  in  the  pulp  chamber  and  in  root  canals. 
In  these  nodules  occasionally  calcospherites  are  found.  In  some 
instances  the  pulp  contains  in  the  root-canal  portion  a  number 
of  nodnles  which  are  accountable  for  the  so-called  lead-wire  for- 
mation, as  described  by  Black.  Here  also  erosion  and  abrasion  are 
frequently  the  cause  of  pulp  nodules.  The  number  and  size  of 
pulp  nodules  vary.  In  some  microscopic  sections  examined  by 
the  author  as  many  as  fifty  pulp  stones  were  counted  in  one  field 
of  a  pulp. 


chapter  xli 
pulp  hyperemia 

General  Considerations 

By  pulp  hyperemia    is  understood  an  abnormal  condition   in 
which  the  vessels  of  the  pulp  are  engorged.     The  organ  in  most 

of  the  cases  is  the  seat  of  active,  rather  than  of  passive,  conges- 
tion, and  responds  to  thermal  stimuli  with  a  degree  of  intensity 
more  pronounced  than  is  normal  to  it.  The  congestion  is  brought 
about  either  by  paralysis  of  the  vasoconstrictor  nerves  of  the 
blood  vessels  of  the  pulp,  or  by  stimulation  of  the  vasodilators, 
following  the  infliction  of  degrees  of  irritation.  (I.  V.  Black' 
was  of  the  opinion  that  all  pulp  hyperemias  are  active  or  ar- 
terial, while  Hopewell- Smith2  argues  that  venous  hyperemia  of 
the  pulp  occurs  more  frequently  than  arterial.  From  the  clinical 
standpoint  this  diversity  of  views  has  no  significance  whatsoever. 
Hyperemia  proper  is  to  he  segregated  from  that  hyperemia  which 
is  one  of  the  phenomena  of  pulp  inflammation,  the  former  being 
considered  here  as  a  distention  of  the  vessel  walls  independent 
of  any  reaction  to  septic  invasion  (Figs.  421  and  422).  It  is 
practically  in  all  instances  of  the  active  type;  that  is  to  say,  the 
beginning  is  marked  by  changes  in  the  caliber  of  the  pulp  arteries 
and  in  the  quantity  of  blood  which  they  hold.  It  must  be  noted, 
however,  that  as  the  result  of  a  distention  of  the  arteries  and  their 
increased  blood  contents  there  occurs  a  corresponding  decrease 
in  the  lumen  of  the  veins — a  purely  mechanical  cause  which  we 
interpret  as  the  inability  of  the  veins  to  drain  increased  blood 
supply,  because  of  their  limited  power  of  accommodation,  limited 
as  it  is,  to  overcome  exaggerated  arterial  pressure  within  tin1 
pulp.  The  pulp  mass  must  continue  constant  on  account  of  the 
unyielding  character  of  its  surroundings  (the  walls  of  the  pulp 
chamber  and  root  canals"),  so  that  a  dilatation  of  one  set  of  ves- 
sels— the  arterial — must  be  synchronous  with  a  compression  of 
the  other — the  venous. 


•Black,   G.   V.:      Special   Dental    Pathology.   Chicago,   Medico-Dental   Pub    Co 
=Hopewell-Smith,  A.:      In    X.    G.    Bennett's    Science   and    Practice   of    Dental    Surgery 
New    York,   Wm.    Wood   \   Co  " 

518 


ITU'    HYPEREMIA 


519 


Etiology 

The  causes  of  pulp  hyperemia  are,  indirectly,  all  disease 
processes  or  forces  responsible  for  a  decrease  in  either  the  thick- 
ness or  density,  or  both,  of  the  protecting  tissues  of  the  pulp.  The 
direct  causes  are  the  subjection  of  the  pulp  to  stimuli  of  a  de- 
gree of  intensity  greater  than  is  normal   for  thai   pulp.     In  hy- 


h'ig.  421. — Section  of  dental  pulp,  longitudinal.  The  distention  and  congestion  of  the 
vessels  in  the  course  of  hyperemia  is  here  beautifully  shown.  With  the  exception  of  the 
abnormal  caliber  of  the  vessels  all  the  other  tissue-elements  are  of  normal  appearance. 
u,  a,  a.  a,  distended   vessels;    b,  b,   odontoblastic   layer. 


peremia  of  the  pulp,  the  bacterial  factor  is  excluded,  except  when 
indirectly  induced  by  dental  caries,  when  the  destruction  of 
portions  of  the  enamel  and  of  the  dentin  bring  about  irritation 
of  the  pulp  by  permitting  the  transmission  of  thermal  impulses, 
which  in  the  case  of  a  sound  tooth  would  not  occur.  Also 
it  should  be  noted  that  the  products  <>f  fermentation  and  putrefac- 


520 


DENTAL    PATHOLOGY 


t ion,  especially  when  concentrated,  act  as  irritants  to  the  pulp, 
a  condition  which  occurs  constantly  in  a  carious  cavity. 

The  pulp  of  each  tooth,  as  pointed  out  years  ago  by  Jack,  has 
a  temperature  range  peculiar  to  itself;  a  decrease  of  several 
degrees  of  temperature  in  this  range,  either  from  the  higher  or 
lower  maximum,  is  to  be  interpreted  as  hyperemia.  For  instance, 
if  a  pulp,  under  normal  conditions,  does  not  respond  to  applica- 
tion of  water  of  a  temperature  of  from  98°  down  to  50°   F.,  or 


Fig.  422  — Cross  section  of  hyperemic  pulp.  No  pathologic  lesion  per  se  is  to  be  de- 
tected at  this  stage  of  the  process.  -  Some  few  distended  blood  vessels  containing  large 
n umbers  of  blood  cells  are  seen  on  the  upper  part  of  the  picture,     a,  a,  distended  vessels. 


from  98°  up  to  128°,  such  a  pulp  has  a  temperature  range  of 
78°.  This  plan  suggests  the  advisability  in  all  cases  in  which  the 
possibilities  of  hyperemia  are  brought  into  play  (i.e.  following 
the  insertion  of  metallic  fillings  or  the  preparation  of  teeth  for 
crowns),  to  obtain  the  temperature  range  before  the  hyperemic 
state  develops.  In  the  event  of  painful  symptoms  developing,  by 
ascertaining  whether  or  not  a  decrease  in  the  temperature  range 


PULP    HYPEREMIA  •">_  1 

has  occurred,  a  corred  diagnosis  can  be  more  easily  established, 
and  the  disturbed  pulp  is  definitely  located. 

The  thickness  or  density,  or  both,  of  the  protecting  Tissues  of 
the  pulp  (enamel,  dentin  and  cementum)  are  modified  by  disease 
processes  as  well  as  factors  other  than  these.  Among  the  former 
we  include  dental  caries,  erosion  and  abrasion;  annum'  the  latter, 
the  removal  by  mechanical  means  of  closely  adjacent  portions 
of  the  enamel  or  dentin  preparatory  to  the  restoration  by  crowns 
or  fillings  which  have  much  higher  degrees  of  thermal  conduc- 
tivity (such  filling  materials  as  gold,  or  silver  and  its  alloys). 
Furthermore,  while  per  s<  the  insertion  of  a  small  metallic  filling 
may  not  perhaps  cause  hyperemia,  the  development  of  an  exces- 
sive degree  of  heat  in  the  process  of  polishing  such  a  filling  will 
frequently  bring  about  this  pathologic  disturbance.  Also  the 
presence  of  a  foreign  mass,  such  as  a  filling  of  gold  or  of  amal- 
gam, is  in  itself  irritating  to  the  dentinal  fibrillar. 

Hyperemia  or  congestion  of  the  pulp  may  also  develop  fol- 
lowing fractures  of  portions  of  the  croAvns  of  teeth,  also  follow- 
ing the  traumatisms  incident  to  the  condensation  of  gold  fillings. 
In  the  latter  instance  both  the  peridental  membrane  and  the  pulp 
may  become  affected.  It  may  also  occur  from  the  action  upon 
the  pulp  of  chemical  substances  such  as  formalin,  paraformalde- 
hyde, silver  nitrate,  zinc  chloride,  etc.,  and  from  the  too  rapid 
movement  of  teeth  in  orthodontia. 

The  recovery  from  hyperemia  depends  upon  a  recovery  of 
normal  tone  (contraction)  by  the  vessels  of  the  pulp,  and  is 
governed  by  the  length  of  time  the  hyperemia  has  existed,  the 
frequency  and  intensity  of  the  paroxysms  of  pain,  and  the 
thoroughness  with  which  the  pulp  environment  is  favorably 
changed.  If  the  cause  be  a  metallic  filling,  this  should  be  re- 
moved and  replaced  by  a  filling  of  gutta-percha,  and  the  use  of 
foods  or  beverages  of  too  low  or  too  high  a  temperature  must 
be  most  carefully  avoided.  In  other  words,  the  environmental 
disease-producing  factors  should  be  eliminated  at  once. 

Abrasion  and  erosion  causing  hyperemia,  not  infrequently  neces- 
sitate the  removal  of  the  pulp  if  the  disturbance  is  not  promptly 
relieved  by  such  methods  as  counterirritation  or  the  use  of  co- 
agulant obtundents.  In  the  absence  of  infection  the  pulp  is  capa- 
ble of  fully  recuperating  from  the  effects  of  a  hyperemia.    Black 


522  DENTAL   PATHOLOGY 

has  shown  that  either  moderate  or  relatively  large  liquid  in- 
flammatory exudates  are  disposed  of  successfully  by  the  pulp 
if  placed  under  a  nonirritating  environment. 

The  paroxysms  of  pain  from  pulp  hyperemia  may  last  from 
just  a  few  seconds  to  several  minutes,  or  hours,  or  even  days. 
In  some  cases  the  pain  is  not  exaggerated,  although  continuous; 
in  others  it  is  both  intense  and  continuous, — at  times,  for  a  period 
of  seconds,  the  pain  being  unbearable.  The  pain  may  be  lo- 
calized in  the  affected  tooth,  but  may  be  felt  in  several  teeth  or 
in  the  entire  side  of  the  jaw.  It  may  also  be  of  the  radiating 
type,  i.e.  toward  the  temple,  the  ear,  the  eye,  or  the  forehead. 
Occasionally  a  hyperemia  in  an  upper  tooth — the  cuspid  in  par- 
ticular-— will  be  reflected  to  all  of  the  upper  teeth  posterior  to  it, 
and  sometimes  also  to  a  number  of  teeth  in  the  lower  jaw  of  the 
corresponding  side.  An  intense  hyperemia  with  corresponding 
degree  of  pain,  or  a  moderate  hyperemia  lasting  for  several 
weeks  or  months,  if  permitted  to  go  untreated,  ends  in  the  death 
of  the  pulp;  here  the  hyperemia  has  assumed  the  characteristics 
of  a  nonseptic  pulpitis.  All  pain  having  ceased  the  patient  feels 
greatly  relieved  both  physically  and  mentally ;  but  such  a  dead 
pulp  may  at  any  time  give  rise  to  an  acute  or  a  chronic  alveolar 
abscess,  and  the  chronic  abscess  may  be  either  of  the  frank  type 
with  a  sinus,  or  of  the  blind  type  without  one. 


CHAPTER  XLI] 
GANGRENE  OF  THE  PULP— PUTRESCENT  PULP 

General  Considerations 

By  gangrene  of  the  pulp  (gangrenous  decomposition)  is  meanl 
death  of  the  pulp  en  masse.  It  is  the  resull  of  the  shutting  off 
of  the  circulation  to  the  pulp  through  mechanical,  thermal,  or 
chemical  factors,  or  as  the  result  of  paralysis  of  the  vessel  walls. 
The  shutting  off  of  the  circulation  at  the  apex  may  he  caused 
by  (1)  blows  upon  the  teeth,  (2)  tooth  movement  in  orthodontia, 
(3)  the  quick  separation  of  teeth  preparatory  to  filling  opera- 
tions, or  (4)  nonseptic  pulpitis  leading  to  thrombosis  and  con- 
sequent  infarction.  The  chemical  causes  are  those  incident  to 
the  application  of  so-called  mummifying  or  tannifying  sub- 
stances which  contain  formalin,  tannic  acid,  thymol,  zinc 
chloride,  or  other  tannifying  or  coagulating  substances.  In 
the  latter  group  of  cases,  the  chemical  substances  used  doubtless 
dehydrate  the  pulp,  and  by  disturbing  its  metabolism  to  a  de- 
gree beyond  the  possibility  of  cell  recovery  lead  to  cellular  death 
(necrobiosis)  of  the  pulp  which,  in  the  absence  of  bacteria  and 
because  of  its  complete  dehydration,  remains  in  the  root  canals 
as  a  shriveled  mass. 

Paralysis  of  the  vessel  walls  is  caused  by  any  form  of  shock, 
such  as  in  a  greater  degree  might  cause  the  strangulation  of  the 
pulp  at  the  apex.  It  is  doubtful  whether  a  pulp  dies  because  of 
an  actual  strangulation  (severance)  of  its  blood  vessels.  Instead, 
it  is  more  likely  that  the  injury  to  the  vessel  walls  is  the  cause 
of  a  thrombosis  in  either  the  arterial  or  venous  trunk  of  the 
pulp.  In  other  words,  death  of  the  pulp  follows  a  series  of 
arterial  or  venous  obstructions,  rather  than  a  single  strangula- 
tion. 

The  pulp  which  dies  in  bulk  either  remains  in  a  state  of  dryness 
or  mummification,  or  becomes  infected.  In  the  former  condition 
all  fluids  in  the  pulp  are  absorbed  and  when  the  pulp-chamber  is 
opened  the  pulp  has  a  dried  up,  parchment-like  appearance, 
with  no  offensive  odor  detectable.  In  the  latter  stage  moist 
gangrene   develops. 

523 


f>24  DENTAL    PATHOLOGY 

By  moist  gangrene  is  meant  putrefactive  decomposition  of  the 
pulp,  a  process  identical  to  that  which  occurs  in  the  bodies  of 
dead  animals.  The  bacteria  concerned  in  this  process  are  sapro- 
phytes— bacteria  which  depend  for  their  existence  upon  the  prod- 
ucts of  the  decomposition  of  dead  nitrogenous  matter.  It  is, 
however,  to  be  remembered  that  bacteria,  even  though  parasitic, 
may.  when  circumstances  demand  it,  develop  saprophytic  proper- 
ties. 

The  organisms  which  have  been  found  in  putrescent  pulps  are 
both  saprophytic  and  pathogenic,  and  it  is  more  than  probable 
that  many  forms  are  facultatively  pathogenic  and  saprophytic. 
Long  thread-forms,  leptothrix,  cocci,  bacilli,  spirilla?  and  spi- 
rochetes have  been  found.  Arkovy  found  the  Bacillus  gangrenae 
pulpae,  the  Staphylococcus  pyogenes  albus  and  aureus,  the  Strep- 
tococcus pyogenes  and  the  Bacillus  pyocyaneus. 

The  breaking  down  of  the  tissue  elements  of  the  pulp  is  a 
process  of  simplification  resulting  ultimately  in  the  formation  of 
hydrogen  sulphide,  ammonium  sulphide,  carbon  dioxide,  and 
water.  The  albuminous  substances  are  first  changed  into  pep- 
tones ;  then  such  animal  alkaloids  as  cadaverin,  putrescin,  and 
neuridin  are  formed;  then  nitrogenous  bases  such  as  leucin  and 
tyrosin ;  then  aromatic  products  such  as  indol,  phenol,  and  cresol ; 
and  finally  the  simpler  compounds  H2S,  C02  and  H20. 

In  teeth  the  pulps  of  which  are  undergoing  putrefactive  decom- 
position, or  a  combination  of  suppuration  and  putrefaction,  dis- 
coloration is  liable  to  occur.  In  these  cases  the  discoloration1  is  prob- 
ably due  to  a  combination  of  factors,  such  as  the  formation  of 
compounds  of  iron  and  sulphur  (black  ferrous  sulphide);  to  the 
action  of  hydrogen  sulphide  (an  end  product  of  putrefaction)  on 
hemoglobin,  resulting  in  the  production  of  sulphomethemoglobin; 
and  to  the  decomposition  of  hemoglobin,  as  already  stated,  in  the 
case  of  unexposed  pulps  when  the  seat  of  nonseptic  pulpitis. 

It  has  been  argued  that  possibly  the  combination  of  ammonia 
(an  end  product  of  putrefactive  decomposition,  which  in  the 
presence  of  water  is  changed  into  ammonium  hydroxide)  with 
iron  (liberated  in  the  course  of  the  decomposition  of  hemoglobin) 
is  changed  into  Fe(OH2),  which  upon  being  oxidized  is  changed 

'Kirk,  E.  C:  Discolored  Teeth  and  Their  Treatment.  American  Textbook  of  Opera- 
tive  Dentistry,   Philadelphia,  Lea  &   Febiger. 


G  \N*.i;i  ni:  OF  Tin:  PULP  .V2.~> 

into  I'.-  'Ml  .  ,i  reddish-brown  compound.  This  may  play  a 
pari  in  the  discoloration  of  teeth  whose  pulps  have  under- 
gone putrefactive  decomposition.* 

A  tooth  containing  a  pulp  which  is  the  seat  of  dry  gangrene 
gives  rise  to  no  subjective  symptom.  The  roo1  canals  arc  occupied 
by  a  mass  n\'  dried  up  tissues  which,  upon  being  exposed  to  the 
moisture  and  bacterial  flora  of  the  mouth,  and  to  a  liberal  supply 
of  oxygen  (increased  oxygen  tension  I,  usually  precipitate  within  a 
short  time  an  infectious  apical  pericementitis,  either  acute  or 
chronic. 

Teeth  in  which  the  pulps  have  died  following  nonseptic  causes 
become  the  seal  of  putrefactive  changes  in  the  presence  of: 

1.  Direct  access  to  the  pulp  chamber  fas  through  carious  cav- 
ities, etc). 

2.  Indirect  access  to  the  pulp  chamber: 

(a)  From  under  a   defective  filling. 

(b)  From  under  a   sound  filling  in  a   cavity  from 
which  all  carious  matter  had  not  been  removed. 

(c)  From  infected  dentinal  tubuli. 

(d)  Through  imperfections  in  the  enamel. 

(e)  Through  cementum  and  dentin  at  the  neck  of 
the  tooth  following  caries. 

3.  By  an  infection  which  has  reached  the  pulp  via  the  circula- 
tion. 

Pulpitis 

Pulpitis,  in  a  general  way.  may  be  defined  as  the  aggregate 
of  inflammatory  phenomena  in  the  dental  pulp,  which  may  be 
either  bacterial  or  nonbacterial  in  origin ;  it  is  distinguished  from 
hyperemia  in  that  the  latter  disease  occurs  in  the  absence  of 
bacterial  irritation  and  subsequent  tissue  destruction — two  char- 
acteristic phenomena  of  pulpitis.  This,  of  course,  fails  to  hold 
good  if  the  hyperemia  is  of  such  severity  as  to  assume  the  charac- 
teristics of  an  inflammation. 

Nonseptic  Pulpitis 
A  nonseptic  pulpitis  is  the  result  of  subjecting  the  pulp  to  an 
exaggerated  degree  of  the  conditions  responsible  for  the  onset 
of  hyperemia.     An  untreated  hyperemia,  in  some  instances,  be- 

*Buckky.  T.  P.:  Modern  Dental  Materia  Medica,  Therapeutics,  and  Pharmacology, 
Philadelphia,  P.  Ijlakiston's  Son  &  Co. 


526  DENTAL   PATHOLOGY 

comes  a  nonseptic  pulpitis  and  ends  in  death  of  the  pulp.  The 
difference  between  nonseptic  pulpitis  and  hyperemia,  from  the 
standpoint  of  pathologic  anatomy,  is  that  in  nonseptic  pulpitis 
occurs  a  diapedesis  of  leucocytes  with,  when  very  acute,  a  trans- 
migration of  a  few  erythrocytes  and  a  transudation  of  serum ;  while 
in  hyperemia  diapedesis  does  not  occur,  although  occasionally  a 
small  number  of  erythrocytes  are  forced  through  the  vessel  walls. 
In  traumatic  pulpitis  the  destruction  of  tissue  by  proteolysis 
does  not  occur.  The  pulp  cells  die  following  the  shutting  off  of 
the  circulation  of  the  organ  by  thrombi,  or  by  the  products  of 
cell  degeneration,  fat,  cell  fragments,  etc.  If  the  pulp  remains 
free  from  bacteria  the  tooth  will  remain  comfortable,  usually 
until  such  time  as  an  attempt  is  made  to  remove  the  dead  con- 
tents of  the  root  canal,  when  not  infrequently  a  dentoalveolar 
abscess  develops  as  the  result  of  the  passage  through  the  apical 
foramen  into  the  periapical  tissues  of  the  products  of  putrefac- 
tive decomposition  and  of  bacteria;  and  also  of  a  change  in  oxy- 
gen tension  in  the  root  canals. 

Septic  Pulpitis 

The  pulp  is  very  susceptible  to  the  effects  of  bacterial  invasion, 
and  being  possessed  of  a  minimum  of  recuperative  powers,  be- 
comes without  delay  the  seat  of  a  destructive  inflammation  upon 
being  subjected  to  even  the  mildest  degree  of  bacterial  infection. 
The  virulence  and  number  of  the  bacteria  and  the  degree  of  vital 
resistance  of  the  tissues  of  the  pulp  determine  whether  the  in- 
fection will  pursue  a  rapid  course  with  proportionate  rapid  tissue 
destruction,  or  whether  the  course  will  be  slow  and  the  destruc- 
tion of  the  pulp  will  consume  a  longer  period  of  time.  Acute- 
ness  and  chronicity  are  differentiated  from  the  standpoint  of  the 
duration  of  the  inflammatory  process  up  to  the  time  of  the  death 
of  the  pulp.  While  determined  clinically  in  most  cases  by  the 
severity  or  mildness  of  the  pain,  together  with  the  period  of  time 
the  pain  has  been  present,  this  symptom  is  not,  however,  in  all 
cases,  a  true  index  of  the  degree  of  infection.  In  some  cases  in 
which  death  of  the  pulp  occurs  in  a  short  time  following  an  in- 
fection, the  pain  is  neither  severe  nor  paroxysmal,  but  rather 
mild  and  practically  continuous,  ivhich,  bearing  in  mind  our 
clinical  diagnosis,  would  be,  as  far  as  the  degree  of  pain  is  con- 


G  W'.l.TNl     OP   THE    I'ULP  527 

eerned,  indicative  of  chronicity  rather  than  of  acuteness;  and 
again,  in  other  cases  in  which  the  infectious  pulpitis  is  of  long 
duration,  the  pain  may  be  just  as  intense  as  that  which  accom- 
panies the  severer  in  feci  ions,  which  once  more  would  reverse  the 
usual  findings. 

In  the  presence  of  a  wide  opening  by  caries  into  the  pulp  cham- 
ber, even  an  acute  process  of  pulp  destruction  may  not  give 
rise  to  extremely  painful  phenomena,  since  the  inflammatory 
exudates  find  an  outlet  into  the  cavity  of  decay,  so  that  the  pres- 
sure within  the  pulp  Avill  at  no  time  reach  the  maximum — unless 
it  be  when  the  exposure  becomes  obstructed  with  food  debris. 
To  the  contrary,  an  inflammatory  process  by  less  virulent  organ- 
isms in  the  pulp  chamber  or  root  canals,  in  the  absence  of  drain- 
age, may  <jive  rise  to  very  intense  pain,  as  occurs  when  the  open- 
ing into  the  pulp  chamber  through  an  unfilled  cavity  becomes 
clogged  with  food  debris,  or  when  a  slowly  progressive  infectious 
pulpitis  develops  following  the  insertion  of  a  filling.  The  pain 
factor  is  modified  in  accordance  with  conditions  which  favor  or 
prevent  maximum  degrees  of  pressure.  These  must  be  borne  in 
mind  and  looked  to  in  making  a  diagnosis.  Chronic  infectious 
pulpitis  is  the  exception  rather  than  the  rule. 

In  pulps  containing  the  products  of  suppuration  in  the  shape 
of  extra vasa ted  serum,  liquefied  pulp  cells,  and  liquefied  leu- 
cocytes, cells  partially  or  completely  disorganized,  the  reactions 
to  cold  applications  decrease  the  existing  pain,  while  the  re- 
actions to  heat  applications  are  very  marked.  In  the  wake  of 
the  suppurating  process  a  putrefying  process  may  be  following, 
and  the  gaseous  end  products  expanding  under  heat  increase  the 
pressure  against  the  peridental  membrane  in  the  apical  area  and 
against  the  medullary  substances  in  the  adjoining  cancellated 
spaces.  There  is  also  a  sense  of  pressure  in  the  tooth  and  in  the 
tissues  overlying  it.  and  pain,  which  varies  in  severity  according 
to  whether  the  inflammatory  exudates  remain  enclosed  in  the 
root  canals  or  are  discharged  through  an  exposure  into  a  carious 
cavity. 

The  infection  of  a  pulp  by  pyogenic  bacteria  may  occur  in  the 
complete  absence  of  caries,  the  infection  traveling  in  the  peri- 
dental membrane,  perhaps  following  a  chain  of  epithelial  rem- 
nants, or  coming  from  the  seat  of  septic  apical  pericementitis  in 


528  DENTAL   PATHOLOGY 

a  neighboring  tooth;  and  again,  a  tooth  which  is  the  seat  of 
chronic  nonseptic  pulpitis  may  become  the  seat  of  septic  pulp- 
itis, when  the  evidence  points  to  the  entrance  of  bacteria  into 
the  pulp  via  the  circulation.  Dental  caries  may  have  progressed 
so  far  as  to  frankly  expose  the  pulp;  or  the  infection  may  ante- 
date the  exposure,  in  which  case  the  bacteria  have  penetrated 
through  the  dentinal  tubuli  into  the  pulp.  In  young  teeth  in 
which  the  diameter  of  the  tubuli  is  relatively  larger,  the  chances 
of  infection  of  the  pulp  by  the  passage  of  bacteria  through  them 
is.  of  course,  greater.  But  caries  is  not  the  only  cause  of 
pulpitis.  In  advanced  pyorrhea  the  infectious  process  may  reach 
the  apical  tissues  and  involve  the  pulp ;  also  a  peridental  infec- 
tion in  a  neighboring  tooth  may  spread  so  as  to  involve  the  pulps 
of  adjacent  teeth.  Pulpitis  is  characterized  by  changes  in  the 
dental  pulp  similar  to  changes  which  occur  in  other  tissues  of 
the  body  as  the  result  of  an  infectious  inflammation.  Pulpitis 
may  result  in  the  complete  disorganization  of  the  pulp. 

In  eases  of  pulp  suppuration  the  tissue-cells,  which  have  died 
consequent  upon  the  action  of  the  pyogenic  bacteria  and  their 
toxines,  may  become  the  seat  of  putrefactive  decomposition  with 
manifestations  identical  to  those  which  develop  in  the  case  of 
moist  gangrene  of  the  pulp.  A  pulp  which  has  died  following  a 
traumatism  or  the  action  of  chemical  agents,  in  the  absence  of  a 
direct  or  indirect  exposure,  may  remain  quiescent  for  a  long  time 
and  then  become  the  seat  of  putrefaction  and  its  sequelae. 

Pathologic  Anatomy 

Following  the  presence  in  the  pulp  of  bacterial  exciters,  the 

arteries  at  first  contract  for  a  very  short  time.  This  contraction 
is  then  followed  by  a  dilatation  affecting,  in  the  order  given, 
arteries,  veins  and  then  capillaries.  The  blood  current  is  now 
temporarily  accelerated,  but  by  the  time  the  dilatation  of  vessels 
is  complete,  this  temporary  acceleration  is  changed  into  a  pro- 
gressive retardation.  Leucocytes  adhere  to  the  vessel  walls;  the 
axial  circulation  becomes  rich  in  red  blood  cells;  leucocytes  pass 
through  the  vessel  walls  (diapedesis),  and  exudation  of  serum 
takes  place.  The  toxines  of  the  bacteria  kill  and  liquefy  the 
cells  (Fig.  423)  of  the  pulp,  and  these,  together  with  dead  and 
liquefied  leucocytes,  leucocytes  in  various  stages  of  degeneration, 


GANGRENE   OF   THE    PULP 


529 


fixed-tissue  cells  and  serum  exudate,  constitute  the  pus  found  in 
a  pulp  chamber  or  root  canal  in  which  the  pulp  is  succumbing 
to  the  effects  of  a  pyogenic  infection. 


Fig.  -423. —  Longitudinal  section  of  a  dental  pulp,  the  upper  portion  of  which  has  been 
the  seat  of  a  suppuration.  The  hazy  area  in  the  top  of  the  picture  represents  cell 
liquefaction.      Focusing   did    not   change   the   appearance. 


The  reparative  power  of  the  pulp  being  practically  nil,  the  in- 
fectious process  will  advance  uninterruptedly,  in  practically  all 
cases,  until  the  entire  organ  is  destroyed. 


530  DENTAL   PATHOLOGY 

The  infection  of  the  pulp  may  assume  the  ulcerative  form  or 
the  circumscribed  form — pulp  abscess.  In  the  former  instance 
the  pulp  exhibits  no  tendency  to  circumscribe  the  infection 
which  proceeds  until  the  entire  organ  is  destroyed,  and  may 
spread  to  involve  the  periapical  tissues  and  give  rise  to  an 
acute  or  chronic  dentoalveolar  abscess.  In  the  latter  instance  a 
condensation  of  inflammatory  cells  (round-cell  infiltration)  takes 
place.  A  degree  of  resistance  of  the  pulp  almost  equal  to  the 
degree  of  virulence  of  the  infection  is  responsible  for  the  suc- 
cessful efforts  to  partially  ward  off  the  infection. 

Clinically  the  pulp  abscess  and  the  uncircumscribed  infection 
are  not  distinguishable.  The  symptoms  may  be  equally  severe 
in  both  conditions. 

The  discoloration  of  a  tooth  whose  pulp  has  not  been  exposed 
to  bacterial  influence  through  an  opening  in  the  pulp  chamber 
(absence  of  caries),  but  lias  been  the  seat  of  an  acute  inflamma- 
tion leading  to  the  formation  of  thrombi  and  emboli  and  to 
hemorrhagic  infarcts,  is  due  to  the  impregnation  of  the  dental 
tubuli  and  dentin  matrix  with  the  products  of  the  hemolysis  of  the 
erythrocytes  in  the  extravasated  blood  serum.  The  tooth  assumes 
at  first  a  pinkish  hue,  which  may  be  very  light.  In  time,  after 
going  through  a  series  of  discolorations,  such  as  yellow,  brown, 
and  slaty-gray,  it  may  become  even  black,  due  to  the  progressive  de- 
composition of  the  hemoglobin,  forming  methemoglobin  (brown- 
ish red),  hemin  (bluish  black),  hematin  (dark  brown  or  bluish 
black),  or  hematoidin  (orange),2  either  alone  or  in  combinations. 

Pulp  Hypertrophy 

Pulp  hypertrophy  is  the  result  of  a  combined  bacterial  and 
mechanical  irritation.  The  pulp  as  a  whole  has  been  infected 
by  bacteria  of  a  low  degree  of  virulence  for  a  prolonged 
period  of  time.  It  is  a  chronic  infectious  process  in  the  pulp. 
This  slow  inflammation  results  in  the  proliferation  of  fixed-tissue 
cells  into  masses  of  embryonic  (granulation)  tissue.  The  enlarge- 
ment of  the  pulp  continues  as  long  as  the  degree  of  irritation  per- 
sists. 


=Kirk,   E.   C. :     Discolored   Teeth   and   Their   Treatment,   American   Textbook   of   Opera- 
tive  Dentistry,   Philadelphia,   Lea   &   Febiger. 


(i  \n<;ki:\k  of  THE  PULP  53] 

To  this  bacteria]  irritation  there  may  in  time  be  added  ;i  me- 
chanical one,  caused  by  the  impingemenl  of  the  enlarged  pulp 
upon  llif  edges  of  an  exposure.  The  vascularity  of  an  enlarged 
or  hypertrophied  pulp,  and  that  of  protruding  gum  (issue,  is 
about  equally  active.  The  sensitiveness  is  variable,  in  some  wises 
the  enlargement  being  entirely  devoid  of  nerve  filaments.  Sensi- 
tiveness in  these  eases  is  apparent  only  after  removal  of  the  bul- 
bous section  of  the  pulp. 

Visible  pulp  hypertrophy  can,  of  course,  exist  only  in  the  pres- 
ence of  an  aperture  leading  into  a  cavity  of  caries.  Black  has 
described  cases  in  which  a  hypertrophied  pulp  has  been  accom- 
panied by  resorption  of  the  dentin.  The  replacement  of  portions 
of  the  odontoblastic  layer  by  giant  cells  has  been  observed  in 
connection  with  chronic  inflammations  of  the  pulp.  Perhaps 
these  giant  cells  are  present  in  conjunction  with  pulp  hyper- 
trophy in  those  instances  in  which  absorption  of  areas  of  dentin 
occurs.  It  may  also  be  possible,  as  it  has  been  recently  observed 
in  the  case  of  bone  resorption,  that  there  takes  place  an  infiltra- 
tion by  leucocytes  which  assume  osteoclastic  functions  and, 
through  breaks  in  the  odontoblastic  layer,  come  into  contact  with 
the  dentin,  causing  its  resorption  in  limited  areas. 

Occasionally  these  hypertrophic  changes  in  the  dental  pulp 
are  associated  with  calcareous  formation;  within  the  enlarged 
organ.  The  bulk  of  an  enlarged  or  hypertrophied  pulp  is  made 
up  of  granulation  tissue  which  in  time  may  change,  all  or  a  por- 
tion of  it,  into  fibrous  tissue.  Occasionally  the  periphery  of  a 
hypertrophied  pulp  will  present  cellular  elements  resembling 
epithelial  cells,  the  origin  of  which,  if  they  are  really  epithelial 
cells,  is  certainly  obscure. 


CHAPTER  XLIII 

CYSTIC  ODONTOMAS 
By  G.  B.  New,  M.B.,  Mayo  Clinic,  Rochester,  Minn. 

( Vstic  odontomas  will  be  considered  under  two  classes — the 
simple  cysts  and  the  adamantinomas.  The  single  cysts  are  again 
divided  into  two  types:  Type  A,  including  the  cysts  commonly 
called  dental  or  root  cysts;  and  Type  B,  those  usually  called 
follicular  cysts,  and  containing  a  partially  formed  tooth.  The 
term  "follicular"  cysts  used  for  the  second  type  is  misleading 
in  that  one  takes  for  granted,  without  knowing  definitely,  that 
this  type  is  developed  from  the  follicle  of  a  tooth.  The  term 
"dentigerous"  cyst  is  used  quite  loosely  and  may  refer  to  either 
of  the  foregoing  types  of  simple  cysts.  For  this  reason  it  has 
not  been  used  in  this  classification. 

Twenty-six  cystic  odontomas  are  herein  reported  from  the 
Mayo  Clinic.  Twelve  of  these  are  simple  cysts  of  Type  A;  six 
are  of  Type  B;  and  eight  are  adamantinomas. 

Simple  Cysts  of  Type  A 
The  simple  cysts  (Type  A)  are  the  most  common  cysts  of  the 
jaws.  Because  of  their  little  surgical  importance,  they  have  not 
received  the  attention  which  has  been  given  to  other  cystic  odon- 
tomas. Magitot,1  in  1872,  published  the  first  important  work  on 
the  subject  of  cystic  odontomas,  and  attributed  their  origin  to  the 
development  of  the  embryonic  dental  tissue.  Malassez,2  in  1885, 
found  masses  of  cells  about  the  roots  of  teeth  in  the  jaws  of 
adults  and  concluded  that  these  were  the  remains  of  the  dental 
ridge,  the  epithelial  cord,  and  the  outer  layer  of  the  enamel  or- 
gan. These  cells  may  be  found  near  the  teeth  and  are  sometimes 
found  deep  in  the  jaws.  Malassez  called  these  masses  of  cells 
debris  epithcliauf  dentaires,  and  proposed  the  theory  that  all  cystic 
odontomas  were  derived  from  this  group  of  cells.  This  theory 
is  the  one  most  commonly  accepted. 


1Magitot:      Arch.    gen.    de    med.,    1S72,   p.    339. 

2Malassez:     Arch,   de  physiol.   norm,   et  path.,    1885,   p.    129. 

532 


CYSTIC    ODONTOM  \S 


533 


According  to  Scudder,8  this  type  of  cysl   is  round  more  com- 
monly  in  the  upper  jaw  in  the  incisor  and  bicuspid  regions.    Of 

the  twelve  cysts  of  this  series,  six  occurred  in  the  upper  jaw  and 
six  in  the  lower.  Of  those  in  the  upper  jaw  four  occurred  in  the 
incisor  region,  one  in  the  bicuspid  region,  and  in  one  case  the  lo- 
cation was  not  noted.  In  the  lower  jaw  three  occurred  in  the 
incisor  region,  two  in  the  bicuspid  region,  and  one  in  the  molar 
region. 


Fig.   424.      (New.) 

The  typical  mammalian  dentition  consists  of  forty-four  teeth; 
and  man  has  but  thirty-two,  a  third  incisor,  a  third  bicuspid  and 
a  fourth  molar  being  missing.  The  most  frequent  location  for  the 
appearance  of  supernumerary  teeth  is  in  the  upper  jaw  in  the 
incisor  and  bicuspid  regions.  Whether  these  teeth  are  a  rever- 
sion to  the  earlier  types  in  the  mammalian  dentition,  or  simply 
mishappenings,  is  a  questionable  point  among  those  who  have 
made  a  thorough  study  of  the  subject.  It  is  interesting  to  note 
that  this  type  of  cyst  and  the  supernumerary  teeth  most  fre- 

3Scudder:      Tumors    of    the   Jaw,    Philadelphia,    W.    B.    Saunders    Co.,    1912. 


534  DENTAL   PATHOLOGY 

quently  occur  in  the  same  location,  which  might  suggest  that 
these  cysts  are  derived  from  supernumerary  embryonic  centers. 

The  theory  has  been  held  for  some  time  that  these  cysts  develop 
from  irritation  or  stimulation.  The  irritating  factor  may  he  the 
eruption  of  a  tooth  or  some  form  of  peridental  inflammation.  These 
cysts  are  frequently  found  in  connection  Avith  the  dead  roots  of 
teeth,  and  thus  the  irritative  factor,  necessary  to  stimulate  their 
growth,  is  accounted  for. 

Simple  cysts  of  Type  A  occur  at  almost  any  age.  Of  the  twelve 
cases  reported  in  this  chapter,  the  youngest  patient  was  12  years 
of  age  and  the  oldest,  70.  The  cyst  is  usually  about  the  size  of 
an  English  walnut,  but  may  attain  great  dimensions,  and  in  the 
upper  jaw.  simulate  an  empyema  of  the  antrum.  In  the  lower 
jaw  it  may  become  as  large  as  an  orange.  The  cysts  from  our 
series  varied  in  size  from  that  of  a  cherry  to  that  of  a  small 
lemon.  Tumors  the  size  of  a  pea  and  smaller,  are  occasionally 
found  about  extracted  teeth.  They  were  placed  sometimes  near 
to,  and  sometimes  distant  from,  the  root  of  the  tooth.  They  con- 
tained fluid  and  had  an  epithelial  lining  indistinguishable  from  a 
larger  cyst.  The  cysts  have  a  smooth  mucous  membrane  covering 
in  the  mouth:  the  wall  varies  in  thickness  and  consists  of  a  thin 
shell  of  bone  (Fig.  424). 

Simple  Cysts  of  Type  B 

Malassez  believes  that  this  type  of  cysts  also  originates  from 
cells  that  he  describes  in  the  jaws.  Bland-Sutton,4  however,  be- 
lieves that  this  type  simply  represents  an  expanded  tooth  follicle. 

These  cysts  occur  in  either  jaw  with  about  equal  frequency, 
and  usually  in  the  bicuspid  and  molar  regions. 

Of  the  six  cases  in  our  clinic,  three  were  found  in  the  upper 
and  three  in  the  lower  jaw.  Of  the  three  in  the  upper  jaw,  one 
occurred  in  the  bicuspid  region,  one  in  the  molar  region,  and  in 
one  case  the  location  was  not  noted  in  the  history.  Of  the  three 
in  the  lower  jaw,  one  occurred  in  the  bicuspid  region,  one  in  the 
anterior  part  of  the  jaw  and  one  in  the  molar  region. 

This  type  of  cysts  occurs  during  or  shortly  after  the  second 
dentition — except  those  in  connection  with  the  third  molar,  which 
develop  later  in  life.    Although  this  fact  is  commonly  known,  this 


4Bland-Sutton:     Tumors,   Innocent  and   Malignant,   New    York,   Cassel   &   Co.,   1901. 


CYSTIC    ODONTOMAS  535 

type  of  cysts  may  no1  cause  symptoms  or  be  noticed  until  later 
in  adult  life. 

Of  our  cases,  other  than  those  in  which  the  cysl  occurred  in 
the  third-molar  region,  the  ages  of  the  patients  were  3,  14  and 

28  years;  of  those  in  the  third-molar  region,  the  ayes  were  27, 
34  and  37  years. 

It  is  noted  that  a  tooth  is  missing  from  the  set  and  a  partially 
developed  one  is  found  in  the  cavity  of  the  cyst.  The  crown  of 
the  tooth  is  usually  complete  and  the  root  partially  formed.  These 
cysts  occur  about  a  partially  developed  permanent  tooth  and  are 
rarely  seen  about  a  supernumerary  tooth. 

In  one  of  our  cases  the  cyst  occurred  in  a  man  69  years  of  age. 
He  had  had  a  tumor  of  the  lower  jaw  near  the  angle  for  forty- 
two  years,  and  during  the  last  six  months  it  had  increased  in 
size  and  the  surface  had  become  ulcerated  in  the  mouth.  The 
roentgenogram  showed  a  cyst  with  a  partially  developed  molar 
tooth.  A  specimen  from  the  cyst,  on  microscopic  examination, 
proved  it  to  be  epithelioma.  The  extensiveness  of  the  growth 
and  the  glandular  involvement  made  the  condition  inoperable. 

This  type  of  cyst  has  similar  characteristics  as  to  size  as  the 
cysts  of  Type  A.  The  wall  consists  of  thin  bone  and  the  mucous 
membrane  covering  in  the  mouth  is  quite  smooth. 

Adamantinomas 

The  adamantinomas,  on  account  of  their  greater  surgical  im- 
portance and  their  interesting  features  pathologically,  have  given 
rise  to  more  study  than  the  other  types  of  cysts.  It  has  been  held 
that,  in  the  formation  of  enamel  organs  for  the  several  teeth, 
there  was  a  surplus  of  those  formed  and  that  these  additional 
dental  germs  were  the  origin  of  the  adamantinomas.  Malassez' 
ttieorij  as  to  their  development  from  the  epithelial  masses  found  in 
the  jaws  is  accepted  by  most  observers.  Kruse  agrees  with  Ma- 
lassez as  to  the  origin  of  the  cysts,  and  reports  three  cases,  each 
one  typifying  different  stages  in  the  development  of  the  cells  of 
the  enamel  organs.  Biichtemann  and  Kolaczek  believe  that  these 
tumors  originate  from  the  mucous  membrane  or  from  the  mucous 
glands  of  the  mouth.  Bland-Sutton  and  others  hold  that  they 
are  formed  from  the  oral  mucous  membrane.  Bland-Sutton's 
argument  against  Malassez'  theory  is  that  they  occur  in  middle 


536 


DENTAL    PATHOLOGY 


life  and  that  if  they  were  derived  from  the  embryonic  enamel 
organ,  they  would  occur  at  an  earlier  period  in  life. 

Thi   adamantinomas  are  most  frequently  seen  in  flic  lower  jaw. 

Lewis"'  states  that  they  are  seen  eleven  times  more  frequently  in 
the  lower  than  in  the  upper  jaw.  The  bulk  of  the  tumor  mass  is 
usually  at  the  angle  of  the  jaw  extending  upward  to  the  ramus 
and  forward  into  the  body  of  the  jaw.  Sometimes  the  entire 
ramus  is  cystic  with  the  tumor  extending  across  the  mid-line  to 
the  other  side  of  the  jaw.  These  tumors  may  originate  in  the 
molar  or  bicuspid  regions,  but  are  rarely  seen  originating  from 
about  the  anterior  teeth  (Figs.  425  and  426). 


New.) 


I  have  been  able  to  collect  nine  cases  in  which  the  tumor  oc- 
curred in  the  upper  jaw,  two  from  the  Mayo  Clinic.  In  only  four 
of  the  cases  reviewed  in  the  literature  were  there  definite  data 
as  to  the  location  in  the  jaw.  Four  of  the  nine  occurred  in  the 
posterior  part  of  the  jaw  and  tAvo  in  the  cuspid  region.  These 
cysts  may  originate  close  to  the  alveolar  border  or  may  start 
from  deep  within  the  jaw.  Of  the  eight  cases  of  adamantinomas 
from  our  clinic  six  occurred  in  the  lower  jaw  and  two  in  the 
upper.     Of  the  tumors  in  the  lower  jaw,  in  four  the  main  mass 

5Le\vis:      Surg.,    Gynec,   and   Obst.,    1910,   p.   28. 


CYSTIC    ODONTOMAS 


.»:;< 


was  Located  in  the  angle  of  the  jaw,  in  one  in  the  molar  region, 
and  in  one  in  the  bicuspid  region.     Of  those  in  the  upper  jaw, 

one  occurred  well  back  in  the  molar  region  and  one  in  the  cuspid 

region. 

These  cysts  may  develop  at  any  age.  Massin  reports  a  ease  in 
a  new  born  infant,  and  cases  have  been  reported  late  in  adult 
life.  Lewis  states  that  the  average  age  of  the  patients  in  the 
seventy   cases  which   he   collected   in  the  literature,  was  thirty- 


Fig.  426. — (23705).  Roentgenogram  of  case  in  Fig.  425,  showing  entire  absence  of 
ramus  of  jaw  on  right  side  and  the  tumor  extending  across  midline  to  bicuspid  region 
on    left   side.      (New.) 

three.  The  average  age  of  the  patients  in  our  group  of  cases  is 
twenty-seven  and  one-fourth  years.  Of  the  six  eases  from  the 
literature,  in  which  the  tumor  occurred  in  the  upper  jaw,  the 
average  age  of  the  patients  with  occurrence  in  the  molar  region 
was  thirty-three  and  one-half  years,  and  of  those  with  occurrence 
in  the  cuspid  region,  sixteen  and  one-half  years. 

Stumpf  says  that  if  either  of  the  theories  which  have  been  ad- 
vanced for  the  etiology  of  the  formation  of  these  cysts  is  ac- 
cepted, one  must  assume  some  additional  irritant  factor  as  nee- 


538  DENTAL   PATHOLOGY 

essary  in  their  production.  The  lower  molar  region  receives  more 
irritation  than  any  other  locality  in  the  mouth.  It  is  an  accepted 
fact  that  the  lower  third  molar  is  more  difficult  to  erupt  and 
more  frequently  impacted  than  any  other  tooth  in  the  mouth. 
It  is  interesting  to  note  that  it  is  in  this  region  and  at  the 
average  age  of  thirty-three  years — during  or  just  at  the 
time  of  the  eruption  of  the  lower  third  molar — that  these  cysts 
occur.  This  suggests  that  the  eruption  of  the  teeth  may  play  an 
important  part  in  the  chronic  irritation  which  is  probably  neces- 
sary to  stimulate  the  growth  of  these  tumors.  If  these  conditions 
develop  from  supernumerary  embryonic  centers  the  different  lo- 
cations in  the  molar  region  may  be  explained  by  the  fact  that, 
according  to  Black,  the  supernumerary  molar  tooth  may  occur 
in  any  location  posterior  to  the  first  molar.  The  adamantinomas 
are  sometimes  associated  with  cysls  containing  partially  formed 
teeth,  but  not  frequently  enough  to  make  this  a  factor  in  the 
etiology. 

It  is  difficult  to  obtain  conclusive  evidence  of  the  association  of 
the  eruption  and  impaction  of  teeth  to  adamantinomas,  as  most 
histories  are  not  of  sufficient  detail  on  this  point.  Two  of  the 
adamantinomas  in  our  clinic  were  associated  with  unerupted 
third  molars,  one  in  the  upper  and  one  in  the  lower  jaw. 

Of  the  seventy  cases  that  Lewis  collected  from  the  literature, 
the  average  duration  of  symptoms  was  eight  and  one-half  years. 
The  duration  of  the  symptoms  in  our  cases  was  from  ten  months 
to  twenty-one  years.  Most  of  the  cases  were  of  more  than  ten 
years'  duration;  but  the  exact  duration  of  these  tumors  is  diffi- 
cult to  determine  on  account  of  the  long  standing  of  the  condi- 
tion. 

None  of  the  eases  reported  here  had  any  glandular  enlargement. 

These  tumors  present  a  smooth  mucous  membrane  in  the  mouth 
unless  they  are  infected.  The  walls  of  the  cyst  consist  of  a  thin 
laj-er  of  bone.  Crackling  may  be  elicited  in  some  areas,  on  pres- 
sure, where  the  bone  is  thin,  and  fluctuation  may  be  found  in 
others.  These  tumors  may  give  rise  to  great  pain  when  they  are 
of  large  size  because  of  pressure  by  enclosed  fluid.  One  of  our 
patients  who  had  had  a  tumor  for  twenty-one  years,  for  some 
years,  in  order  to  relieve  the  pain,  tapped  the  cyst  herself  as  the 
fluid  accumulated,  by  means  of  a  sterilized  hat-pin. 


CYSTIC    ODONTOMAS 


539 


Pathologic  Anatomy 

The  lining  of  the  simple  cyst.  Type  A,  consists  of  a  layer  of 
fibrous  I  issue  <i  ud  a  thin  layer  of  flattened  epithelial  cells.  In  the 
older  cysts  the  latter  layer  may  not  be  present,  owing  probably 
to  the  pressure  from  the  enclosed  fluid.    Barrie,  in  1905,  reported 


Fig.  427.      (New.) 


a  case  of  dentigerous  cyst  which  was  probably  a  simple  cyst, 
Type  A,  with  typical  adamantine  epithelium,  with  no  down- 
growth,  lining  the  cyst.  This  was  the  first  case  reported  with 
this  type  of  epithelium  forming  the  wall  of  the  cyst. 


f)40 


DENTAL    PATHOLOGY 


The  lining  of  the  simple  cyst,  Type  B,  consists  of  a  fibrous  tis- 
sue layer.  Some  observers  have  reported  an  epithelial  lining  for 
this  type  of  cyst  also. 

The  adamantinomas,  on  section,  present  solid  and  cystic  areas. 
The  cystic  areas  vary  in  size  from  that  of  the  head  of  a  pin  to 
that  of  an  English  walnut.    They  appear  to  have  a  smooth  lining, 


428.     (New. 


and  fibrous  or  bony  septa  are  seen  separating  the  various  cysts. 
The  cysts  contain  a  thin  yellowish  fluid.  The  solid  areas  have  a 
red  tint  and  present  a  granular  appearance,  owing  to  the  many 
minute  cysts. 

Microscopically,  the  solid  areas  consist  of  a  fibrous  tissue 
stroma  and  columns  of  epithelial  cells.  These  columns  may  be 
elongated,  rounded,  or  arranged  in  the  form  of  acini,  and  may 
present  many  irregular  forms.     Two  types  of  epithelial  cells  are 


CYSTIC    ODONTOMAS 


54] 


Fig.  429.     (New.) 


D 


Fig.  430.     (New.) 


542 


DENTAL    PATHOLOGY 


found  in  these  cell  columns:  the  typical  columnar  cells  with  the 
nucleus  placed  near   the  pole  away  from   the   stroma;   and   the 


Fig.  431.      (New. 


Fig.  432.      (New.) 


differentiated  cells  from  this  type — the  polygonal  cell  and  a  stel- 
late cell,  which  form  the  main  mass  of  the  epithelial  columns. 


CYSTIC  ODONTOMAS  543 

These  cells  are  analogous  to  the  cells  thai  form  the  enamel  organ. 
Areas  of  transitional  forms  from  the  solid  cores  to  the  small 
cysts  are  seen.  The  stellate  cells  are  seen  undergoing  disinte- 
gration, their  places  being  taken  by  cyst-cavities,  at  first  quite 
small  and  then  becoming  larger.  Stellate  cells  gradually  dis- 
appear and  are  replaced  by  the  fluid  of  the  cyst.  As  the  cyst  in- 
creases in  size,  the  columnar  cells  are  alone  left  to  line  the  cyst. 
while  in  the  yet  larger  cysts  these  have  disappeared  and  the  wall 
consists  of  fibrous  tissue  only  (Figs.  427-432). 

The  diagnosis  of  the  cystic  odontomas,  when  the  facts  already 
noted  are  considered  and  with  the  aid  of  the  roentgenogram,  is 
usually  not  difficult.  The  roentgenogram  will  show  a  partially 
developed  tooth,  a  unilocular  cyst,  or  the  septa  in  the  multilocu- 
lar  variety.  The  differential  diagnosis  from  a  giant-cell  sarcoma 
is  usually  the  most  difficult,  and  this  has  frequently  to  be  made 
at  the  time  of  operation  or  by  microscopic  examination. 


CHAPTER  XLIV 

MOUTH  INFECTIONS  IX  THEIR  RELATION  TO  SYSTEMIC 

DISEASE 

While  among  the  thinking  practitioners  of  medicine  and  den- 
tistry the  relation  of  month  infections  to  systemic  disease  had 
been  surmised  for  many  decades  past,  it  is  only  within  recent 
years  that  the  subject  has  been  given  proper  scientific  attention 
by  investigators  in  both  professions.  The  investigations  of  the 
late  Miller,  a  pioneer  in  this  as  in  other  fields  of  dental  pathology, 
of  Kirk.  Hartzell.  Henrici.  Moorehead,  Price.  Rosenow,  Billings, 
the  Mayos,  A.  D.  Black,  and  of  the  present  writer  in  collabo- 
ration with  J.  D.  McCoy  and  ('.('.  Browning,  constitute  the  source 
from  which  has  been  abstracted  and  systematized  much  of  the 
information  contained  in  this  chapter.  Hartzell.  in  1908,  pub- 
lished the  result  of  his  observations  on  the  relationship  of  peri- 
apical infections  to  joint  inflammations,  in  which  he  records  the 
improvement  of  the  systemic  condition  following  the  eradication 
by  root  amputations  of  the  infections  in  the  jaws.  William  Hun- 
ter, following  persona]  observations  for  a  period  of  years,  called 
the  attention  of  both  professions  to  the  significance  of  oral  sepsis 
as  an  etiologic  factor  of  many  systemic  disorders. 

The  month,  because  it  is  exposed  at  all  times  to  external  influ- 
ence, and  because  it  affords  all  the  elements  necessary  for  the 
growth  and  multiplication  of  bacteria,  contains  in  both  health 
and  disease  myriads  of  microorganisms  which  are  carried  into 
the  deeper  structures  by  the  blood  or  lymph,  there  to  propagate 
the  moment  the  resistance  of  the  individual  or  of  some  localized 
area  of  tissue  anywhere  in  the  body,  descends  below  the  normal 
for  that  individual. 

In  order  to  have  a  clear  understanding  of  the  pathologic  phe- 
nomena involved  in  the  transportation  of  bacteria  and  bacterial 
toxins  from  the  teeth  to  remote  areas  of  the  body,  a  careful 
study  of  the  histology  and  anatomy  of  the  investing  tissues  of 
the  teeth  and  of  the  osseous  substance  of  the  jaws  is  the  sine  qua 
non.     Nothing  else  will  convey  a  clearer  and  more  definite  idea 

544 


Mor'I'll    INFECTIONS    AND    SYSTEMIC    DISEASE 


545 


of  the  reasons  why  infections  aboul  the  roots  of  the  teeth  can, 
under  qo  circumstances,  be  considered  as  strictly  Localized  proc- 
esses. 

The  blood  supply  of  the  peridental  membrane  and  thai 
of  ilic  surrounding  alveolar  structures  an  not  separati  and  inde- 
pendent vascular  areas.  The  vessels  anastomose  freely  among 
themselves.  An  infeetioB  located  about  the  apex  of  a  root  pro- 
reeds  until  the  cancellated  substance  becomes  involved.  The 
cortical  layer  of  hone  Lining  the  alveolus  soon  breaks  down  as  the 


Fig.  433. — Portion  of  a  mandible  with  cortical  layer  of  bone  removed.  The  relation 
of  the  roots  of  the  teeth  to  the  cancellated  substance  of  the  jaw  is  seen.  The  abundance 
of  blood  vessels  in  the  cancellated  substance  is  responsible  in  some  cases  for  the  arrest- 
ment of  the  infection,  while  in  fortunately  infrequent  instances  it  is  the  reason  for 
severe  metastases. 


result  of  the  infectious  processes  which  develop  in  the  peri- 
apical space,  and  when  this  cortical  layer  disintegrates  the  in- 
fection at  once  reaches  the  cancellated  bone  of  the  alveolar  proc- 
ess, which  is  a  continuation  of  the  cancellated  spaces  of  the  jaw 
proper  (Figs.  433,  434,  and  435).  These  spaces  contain  the 
medullary  substance — a  tissue  richly  supplied  with  blood  vessels 
and  lymphatics.  The  involvement  of  the  alveolar  Avails  is  in  the 
nature  of  a  septic  osteomyelitis.  The  medullary  substance  con- 
tained in  the  cancellated  spaces  becomes  the  seat  of  a  chronic  in- 


546 


DKXTAL    I'ATIIOUHJY 


Fig.  434. — Vertical  gross  section  of  mandible  in  molar  region.  An  abscess  whicb 
develops  in  the  peridental  membrane  of  the  apical  region  soon  involves  this  cancellated 
substance  in  which  blood-vessels  are  numerous  (in  the  myeloid  substance).  Acute  or 
chronic  osteomyelitis   and   metastatic   infections  are   the  probable   results. 


Fig.  435. — Decalcified  transverse  section  of  upper  central  incisors  slightly  above  the 
alveolar  crest  with  intervening  alveolar  process  in  situ.  Following  an  infection  of  the 
peridental  membrane  beginning  at  the  gingiva  the  alveolar  bone  becomes  involved  and 
results  in  a  chronic  osteomyelitis. 


MOUTH    INFECTIONS   AND   SYSTEMIC   DISEASE  547 

Humiliation  in  which  osteoclasts  play  an  active  part.  Through 
osteoclastic  action  the  bard  substance  of  the  hone  disappears. 
the  cancellated  spaces  are  eaten  through,  and  Haversian  canals 
are  widened.  The  contents  of  the  spaces  become  the  seat  of  a 
typical  chronic  inflaiinnal  ion  containing  large  masses  of  small  round 
cells.  The  bone  lamella1  are  successively  destroyed  and  carried  away 
by  osteoclasts,  and  in  time  the  inflamed  medullary  substance  also 
breaks  down.  In  some  places  the  cortical  layer  is  less  than  one- 
third  of  a  millimeter  in  thickness,  and  consequently  it  is  quickly 
broken  down,  thereby  opening  up  an  abundance  of  avenues  for 
the  absorption  of  bacteria  and  bacterial  toxins.  An  acute  or 
chronic  apical  infection  is  practically  at  no  time  a  localized  in- 
fection. If  all  chronic  infections  about  the  roots  of  teeth  do  not 
give  rise  to  systemic  manifestations,  it  is  not  because  the  bacteria 
and  toxins  concerned  in  the  infection  are  not  in  all  cases  at  the 
portals  of  absorption,  but  rather  because  individuals  are  fre- 
quently able  to  ward  off  successfully  a  bacterial  invasion. 

By  the  hematogenic  and  lymphogenic  routes  bacteria  invade 
the  viscera,  muscles,  joints  and  nerve  structures,  and  there  give 
rise  to  any  one  of  a  series  of  pathologic  manifestations.  It  may 
be  a  gastric  or  duodenal  ulcer,  or  an  arthritis,  or  a  myositis,  or 
a  neuritis.  But  it  is  not  only  through  the  hematogenic  and  lympho- 
genic routes  that  systemic  manifestations  of  mouth  infections 
develop.  In  suppurative  diseases  of  the  investing  tissues  of  the 
teeth  (pyorrhea  alveolaris)  in  Avhich  pus  is  constantly  discharged 
into  the  mouth,  systemic  involvement  follows  by  a  combination 
of  (1)  absorption  by  the  blood  and  lymphatic  capillaries  of  the 
gum  and  peridental  membrane,  and  (2)  by  absorption  through  the 
gastric  and  enteric  mucous  membrane  following  the  passage  of  the 
pyogenic  discharges  into  the  stomach.  These  discharges  are  con- 
veyed in  the  saliva,  which  is  constantly  sAvallowed,  and  in  the 
food. 

It  has  been  shown  by  Metchnikoff  that  the  blood  obtained  from 
animals  after  eating,  contains  bacteria,  while  blood  from  animals 
after  fasting  is  sterile.  Miller  showed  some  twenty-five  years 
ago  that  microorganisms  swallowed  in  the  food  and  saliva  are 
not  all  destroyed  by  the  gastric  juice,  estimating  that  eight  out 
of  every  twenty-five  bacteria  swallowed  are  unharmed  by  the 


548  DENTAL    PATHOLOGY 

gastric  juice.  C.  H.  Mayo,1  relying  on  Smithies'  observations, 
refers  to  a  series  of  over  two  thousand  patients  with  gastric  dis- 
orders, in  87  per  cent  of  whom  bacteria  were  found  in  the  stomach 
contents.  Smithies  found  that  "morphologically,  cocci  and  diplo- 
cocci  were  present  in  83  per  cent ;  short  and  long  rods  (often  of 
the  colon  group)  in  58  per  cent;  typical  streptococci  and  staphy- 
lococci in  17  per  cent;  and  leptothrix  buccalis  in  24  per  cent.  In 
fifty-four  cultural  studies  of  the  saliva  from  "dyspeptic"  pa- 
tients, streptococci  and  staphylococci  were  demonstrated  in  over 
80  percent,  bacilli  in  66  per  cent,  and  leptothrix  buccalis  in  more 
than  14  per  cent.  Comparing  these  figures,  it  would  appeal'  that 
the  common  forms  of  pus-producing  organisms  (streptococci  and 
staphylococci)  have  their  proliferation  retarded  in  gastric  juice 
hut  that  bacilli  (often  of  the  colon  group),  as  well  as  leptothrix 
buccalis,  thrive  in  the  stomach.2 

It  stands  to  reason  that  gastric  mucous  membrane  weakened 
by  disorders  due  to  a  gastric  secretion  unsuitable  in  quantity  or 
quality,  or  both;  by  excesses  in  eating  or  drinking,  or  both;  by 
the  retention  of  undigested  food  which  soon  undergoes  putre- 
factive changes;  or  by  any  other  cause — must  lose,  to  some  ex- 
tent at  least,  its  normal  resistance  to  bacterial  influences.  Such 
being  the  case,  a  proportion  of  the  ingested  bacteria  are  bound 
to  incite  both  local  disorders  and  (with  their  entrance  into  the 
capillary  and  lymph  vessels)  inflammatory  disorders  in  any  of 
the  body  organs  or  1  issues  in  which  resistance  to  infection  had 
been  previously  lowered,  and  into  which  the  bacteria  are  carried 
iii  the  blood  or  lymph  streams. 

Oral  foci  of  infection  are  not  the  only  ones  responsible  for  the 
development  of  chronic  maladies;  but  when  present,  the  problem 
of  correcting  these  systemic  disorders  must  also  aim  at  the  elim- 
ination of  the  oral  foci,  regardless  of  any  foci  located  elsewhere 
in  the  body.  The  pendulum,  it  is  claimed,  has  been  made  to 
swing  perhaps  too  far  in  the  direction  of  radicalism;  in  former 
times,  however,  either  through  ignorance  or  caution,  it  had  been 
held  too  far  in  the  direction  of  conservatism.  It  may  be  that  its 
having  reached  what  some  frankly  decry  as  radicalism,  has  out- 
lined a  safe  middle  ground  for  future  practice.    In  that  event  its 


"Mayo,  C.   IF.:     Jour.  Am    Med.   Assn. 

-Ma\u,   C.    II.:     Jour.  Am.   Med.   Assn. 


MOUTH    [NFECTIONS    VND   SYSTEMIC    DISEASE  -"'I!' 

service  has  been  infinite.  In  the  meantime  this  extreme  swing- 
ing is  helping  innumerable  victims  of  empirical  dental  methods 
of  procedure  t<>  discard  the  yoke  of  invalidism,  and  to  regain 
their  respective  places  among  the  useful  units  of  their  communi- 
ties. 

Chronic  mouth  infection — oral  focal  infections — for  the  pur- 
pose of  convenience  in  description  we  have  divided  into  two 
groups;  (1)  the  intraosseous  and  (2)  the  extraosseous.  And  be 
it  understood  thai  by  "oral  focal  infection"  we  imply  an  area 
of  chronic  infection  in  the  mouth — the  teeth  and  its  osseous  and 
sofl  investing  tissues — from  which,  through  hematogenic  or 
lymphogenic  metastases,  chronic  disease  develops  in  any  organ 
or  structure  of  the  body  at  remote  distance  from  the  original 
focus  of  infection. 

In  the  intraosseous  group  are  included  the  chronic  and  subacute 
infections  in  the  substance  of  the  jaws  immediately  adjacent  to 
the  roots  of  the  teeth.  These  are  consequent  upon  a  chronic  in- 
fection of  the  periapical  peridental  membrane — the  sinusless 
chronic  dentoalveolar  abscess  (so-called  dental  granuloma) —  to- 
gether with  the  secondary  foci  of  infection  arising  from  this 
source.  In  the  e  xtraosseous  group  are  included  all  chronic  sup- 
purative diseases  of  the  peridental  membrane,  alveolar  process. 
gingiva  and  gums. 

In  most  cases  of  dental  disease  in  which  extensive  destruction 
of  the  hard  tissues  of  the  tooth  has  taken  place  through  caries, 
with  involvement  of  the  pulp  as  the  consequence,  a  focus  of 
chronic  infection,  if  present,  will,  of  course,  be  located  in  tin1 
deeper  osseous  structures  of  the  jaw.  These  seats  of  chronic  in- 
fection, the  existence  of  which  has  not  altogether  been  unknown  in 
the  past,  have  by  some  been  designated  as  blind  abscesses,  br- 
others, the  author  included,  sinusless  chronic  dentoalveolar  ab- 
scesses, and  by  still  others  denial  granulomas.  They  play  a  very 
active  part  in  the  etiology  of  chronic  inflammatory  disorders  in 
articular  structures,  muscles,  heart,  kidney,  intestines,  etc.  In 
discussing  foci  of  infection  in  the  mouth  we  are  prone  to  give  the 
preference  to  these  septic  nuclei  in  the  deeper  structures  of  the 
jaw  (rarefying  osteitis).  It  is  not  our  aim  to  minimize  their  im- 
portance; nevertheless,  we  feel  constrained  to  state  that  these  are 
not  by  any  means  the  onlv  dental  or  oral  sources  of  o-eneral  in- 


550  DENTAL   PATHOLOGY 

volvement.  Tt  has  been  satisfactorily  shown,  however,  that  infec- 
tion of  joints,  muscles,  the  intestinal  tract,  kidneys,  heart,  etc., 
may  take  place  via  the  hematogenic  or  lymphogenic  routes. 

In  the  month  are  to  he  found  numerous  conditions  which  make 
possible  the  absorption  of  bacteria  and  their  toxins  directly  into 
the  circulation,  in  the  absence  of  "blind  abscesses"- — namely,  in 
the  absence  of  chronic,  acute  or  subacute  pericemental  infections. 
These  extraosseous  sources  of  toxin  absorption  are,  in  patho- 
logic significance,  equal  to,  if  not  greater  than,  the  intraosseous 
focal  areas.  The  presence  upon  the  surfaces  of  the  teeth  of  sali- 
vary calculi  which  maintain  the  margins  of  the  gum  in  a  state  of 
constant  irritation,  either  through  pressure  atrophy  or  through  in- 
duction of  a  suppurative  process,  cause  the  destruction  of  the 
stratified  squamous  epithelium  protective  covering,  and  constitute 
a  prolific  source  of  absorption  of  bacteria — and  bacterial  toxins. 
Almost  invariably,  when  salivary  calculi  are  present  in  varied 
amounts,  such  absorptions  are  going  on  constantly,  not  only  from 
the  locations  in  which  the  calculi  are  present,  but  also  from  ad- 
jacent areas  which  become  involved  by  a  process  of  continuity.  Sal- 
ivary calculi  exert  a  detrimental  influence  upon  soft  tissues  and 
favor  their  invasion  by  bacteria.  They  also  act  mechanically  by 
favoring  the  lodgment  of  food  particles  which,  after  undergoing 
fermentation  or  putrefaction,  or  both,  give  rise  to  either  acid  or 
alkaline  end-products,  which  irritate  the  soft  tissues  and  prepare 
the  field  for  bacterial  invasion  by  decreasing  its  vital  resistance. 
Salivary  calculi  as  a  source  of  bacterial  and  toxin  absorption,  with 
possibly  future  systemic  involvement,  can  not  be  too  strongly 
emphasized. 

The  other  forms  of  calcareous  deposits  upon  the  teeth,  namely, 
those  deposits  which  exist  under  the  free  margin  of  the  gums,  and 
which  are  brought  about  by  some  form  of  irritation  of  the  gingival 
and  septal  tissues,  eventually  lead  to  the  destruction  of  the  peri- 
dental membrane  and  alveolus,  and  likewise  constitute  a  frequent 
source  of  absorption  of  bacteria  and  bacterial  toxins.  Any  form 
of  injury  to  the  gingiva1,  such  as  the  rough  edges  of  crowns  and 
fillings;  negligence  in  the  care  of  the  mouth  permitting  the  accu- 
mulation of  food  particles  which  undergo  decomposition  and  main- 
tain the  gingival  tissues  in  a  state  of  constant  irritation ;  the  pres- 
ence of  unfilled  cavities  of  decay;  defectively  contoured  fillings; 


MOUTH    [NPECTIONS    AND   SYSTEMIC    DISEASE  551 

natural  or  acquired  insufficiency  of  approximal  contact;  and  olhcr 
allied  abnormal  phenomena,  are  all  important  causative  factors  in 
tins  variety  of  deposits.  Subgingival  deposits  invariably  spell  in- 
flammation of  gum  tissue  and  eventually  the  formation  of  pyor- 
rhea pockets.  The  gingiva,  the  peridental  membrane,  and  llic  al- 
veolar process  become  the  seat  of  a  chronic  infection;  the  peri- 
dental membrane  and  the  overlying  alveolar  process  become  tlie 
seat  of  a  destructive  suppurative  inflammation,  slow  in  its  develop- 
ment but,  nevertheless,  one  which  continues  and  in  time  will  lead 
to  the  establishment  of  the  pathologic  condition  which  is  ordinarily 
designated  as  pyorrhea  alveolaris. 

The  importance  of  the  study  of  these  conditions  is  made  more 
understandable  by  recalling-  the  list  of  maladies  which  clinical  ob- 
servation has  shown  to  be  related  in  etiology  to  infections  about 
the  roots  of  teeth  and  their  investing  and  supporting  structures. 
The  list  includes  endocarditis,  myocarditis,  pericarditis,  joint  and 
muscle  infections,  gastric,  intestinal,  renal  and  pulmonary  infec- 
tions, toxemias,  insomnia,  sinus  infections  which  become  secondary 
foci,  etc. 

Hartzell  and  Henrici  have  produced  lesions  of  the  heart,  kidneys, 
aorta,  and  joints  of  rabbits  following  intravenous  injections  of 
8  c.c.  of  a  twenty-four-hour  broth  culture  of  the  strains  of  strepto- 
cocci obtained  from  pyorrhea  alveolaris  and  dentoalveolar  abscess. 

The  mouth  and  teeth,  the  air  sinuses,  the  tonsils,  the  postpharyn- 
geal adenoid  tissue,  upon  becoming  the  seat  of  chronic  infections, 
constitute  jointly  the  most  common  forms  of  focal  infection.  From 
chronic  dentoalveolar  abscesses  and  pyorrhea  alveolaris  have  been 
obtained  different  strains  of  streptococci — the  hemolyticus,  rheu- 
maticus,  and  viridans;  also  the  Staphylococcus  pyogenes  albus  and 
aureus,  the  fusiform  bacillus,  and  the  diplococcus  of  pneumonia; 
and  from  the  saliva  and  pharyngeal  mucus,  in  addition  to  the 
above  are  found  the  B.  diphtheria,  the  B.  tuberculosis,  the  M. 
catarrhalis,  and  a  large  number  of  saprophytic  organisms.  Any 
one  of  these  pathogenic  organisms  may  migrate  into  any  struc- 
ture of  the  body,  as  previously  stated,  by  the  hematogenic  and 
lymphogenic  routes,  and  finding  areas  of  decreased  vital  resist- 
ance, start  on  their  campaign  of  slow  destruction. 

The  Streptococcus  viridans  may  occasionally  produce  acute  in- 
fections even  though  the  organism  is  one  of  low  virulence  and 


552  DENTAL    PATHOLOGY 

brings  about  ehronie  rather  than  acute  inflammations.  Acute 
joint  inflammations  have,  however,  beer  observed  in  which  the 
Streptococcus  viridans  was  the  principal  organism. 

We  now  direct  the  reader's  attention  to  the  advisability  of 
disregarding  the  absence  of  subjective  and  objective  symptoms 
in  the  diagnosis  of  mouth  infections,  having  become  long  ago 
convinced  thai  some  of  the  mosl  pronounced  cases  of  systemic 
involvement  had  developed  in  eases  in  which  there  were  to  be 
found  in  the  mouth  no  indications  of  the  existence  of  a  chronic 
inflammatory  process. 

In  the  course  of  an  investigation  by  James  D.  McCoy,  a  series 
bout  L25  cases  was  radiographed,  several  extra-  and  intra- 
oral exposures  being  made  of  each  ••a-'-,  making  a  total  of  nearly 
500  radiograms.  In  this  series  the  radiograms  showed,  in  each 
instance,  some  theretofore  unsuspected  pathologic  condition,  such 
,i-  impacted  and  incarcerated  teeth,  incompletely  filled  root 
canals,  foci  of  chronic  infections,  etc.  Of  the  cases  exhibiting 
chronic  foci  of  infection  in  each  instance  the  condition  being 
unsuspected  by  the  patient)  a  proportion  of  somewhat  over 
per  cent  had  systemic  manifestations  in  the  form  of  arthritis  or 
myositis  of  various  degrees  of  intensity. 

A  clinical  investigation  covering  a  series  of  125  cases  con- 
stitutes a  strong  enough  nucleus  or'  data  from  which  to  deduct 
conclusions  which  should  lead  to  a  more  definite  conception  of 
the  role  played  by  mouth  infections  in  the  development  of  joint 
and  muscle  inflammation.  The  fact  that  tin'  existence  of  these 
mouth  lesions  had  not  been  suspected  fit  any  time  prior  to  the 
radiographic  examinations,  because  of  absence  of  subjective  and 
objective  symptoms,  is  the  conclusion  in  McCoy's  work  which 
constitutes  a  strong  link  in  tin-  chain  of  evidence  on  the  rela- 
tionship of  month  infections  to  systemic  infections. 

The  Streptococcus  viridans,  an  organism  of  low  virulence,  has 
been  obtained  byHartzell  and  Henrici  from  chronic  dentoalveolar 
abscesses,  and  the  same  investigators3  have  obtained  from 
one  case  of  pyorrhea  alveolari-.  and  dentoalveolar  abscess  various 
strains  of  streptococci,  the  Staphylococcus  albus,  Bacillus  coli, 
Bacillus  proteus,  various  spore-bearing  aerobes  of  the  Bacillus 
subtilis  type,  and  Bacillus  pyocyaneus;  also  ;i  small  Gram-positive 


Am.  Med.  Assn  ,  xliv,  Xo.   13. 


MOUTH    [NFECTIONS    \M>   SYST1  MIC    DISEASE  553 

bacillus  and  a  diphtheroid  bacillus.  Prom  another  case  they  ob- 
tained a  pure  culture  of  Bacillus  fecalis  alcaligenes. 

Urlich  made  au  examination  of  L350  teeth,  82  per  cent  of  which 
showed  apical  abscesses.  He  examined  976  artificially  devitalized 
teeth  with  rod  canal  fillings,  and  of  these  over  68  per  cent 
showed  apical  abscesses.  A  bacterial  examination  was  made  in 
318  cases  and  the  Streptococcus  viridans  and  the  Streptococcus 
hemolyticus  were  found  309  times.  6r  in  97  per  cent  of  all  caves 
examined. 

In  nine  eases  of  acute  arthritis  reported  by  Hartzell  and  Hen- 
rid  in  one  series,  the  patients  showed  marked  improvement  im- 
mediately after  the  removal  of  the  abscessed  teeth. 

In  another  report  they  mention  the  case  of  a  patient  with  pyor- 
rhea alveolaris,  apical  abscess  and  a  severely  painful  arthritis 
which  began  to  recede  a  few  hours  after  the  extraction  of  the 
tooth  having-  the  chronic  dentoalveolar  abscesses.  Cultures  from 
the  root  tip  yielded  another  strain  of  streptococcus  of  high  viru- 
lence, killing  a  rabbit  overnight.  This  rabbit  showed  a  hemor- 
rhage into  one  of  the  mitral  cusps  and  a  number  of  whitish 
streaks  in  the  myocardium  just  beneath  the  pericardium.  In 
these  streaks  were  found,  microscopically,  the  lymphocytes 
gathered  together  in  the  cellular  tissues  under  the  pericardium. 
The  streptococci  were  recovered  in  pure  culture  and  immediately 
injected  in  a  smaller  dose  in  another  rabbit  which  died,  in  two 
days;  the  only  lesions  obtained  in  this  rabbit  were  numerous  mil- 
iary abscesses  in  the  kidneys,  especially  the  medulla — a  case  of 
true  pyemia. 

Hartzell  and  Henrici4  have  also  studied  seven  cases  of  endo- 
carditis. In  two  of  these  patients  the  heart  condition  was  vastly 
improved  by  eliminating  the  mouth  infection. 

One  from  among  the  many  observations  on  the  relation  of  local 
dental  infections  to  arthritis  has  recently  been  reported  by 
Morey.5  In  a  series  of  six  cases  of  arthritis  of  long  standing, 
the  symptoms  subsided  immediately  upon,  or  a  short  time  fol- 
lowing, the  eradication  of  intraoral  foci  of  infection,  the  sup- 
position being  that  the  mouth  streptococcus  had  been  carried 
by  the  hematogenic  route  to  the  points  of  activity  in  the  articu- 


4Hartzell  and  Henrici:     Jour.   National  Dental  Association,  vi,   Xo.    12. 
"•Morey.    F.    L. :     Acting  Assistant    Dental    Surgeon    U.    S.    Navy,    in    the    U.    S.    Xaval 
Medical    l'ulletin. 


554  DENTAL   PATHOLOGY 

lations.  No  attempt  is  made  by  the  reporter  to  connect  all 
cases  of  arthritis  with  diseased  teeth ;  but,  on  the  other  hand,  he 
brings  forth  additional  and  convincing  proof  that  a  large  num- 
ber of  cases  of  arthritis,  nephritis,  cardiovascular  diseases, 
and  inflammations  in  the  gastrointestinal  tract,  are  of  dental 
etiology. 

Three  cases  in  which  infectious  arthritis  were  cured  by  the 
removal  of  teeth  having  a  slight  area  of  infection  are  reported 

by  Morey : 

Case  1 

Arthritis  of  the  right  ankle.  Patient  unable  to  benr  any  weight  on 
his  foot  for  about  six  months;  he  had  been  under  treatment  most  of  the 
time  but  had  not  improved  very  much.  A  roentgenogram  showed  a  slight 
area  of  infection  above  the  right  first  molar,  which  had  only  a  small  occlusal 
amalgam  filling  in  it;  the  patient  was  advised  to  have  the  filling  removed  and 
the  canals  treated,  but  he  preferred  to  have  the  tooth  extracted.  Within  two 
hours  after  the  extraction  the  pain  in  the  ankle  began  to  subside  and  the  next 
day  he  was  able  to  bear  his  weight  on  the  foot. 

Case  2 

Arthritis  of  the  arms  and  legs,  patient  having  been  in  bed  for  four 
months,  some  days  feeling  slightly  improved  but  gradually  growing  weaker. 
No  focus  of  infection  could  lie  found;  a  roentgenogram  of  the  teeth  showed 
a  slightly  infected  area  at  the  root  of  one  of  the  molars.  The  first  molars  had 
gold  crowns  on  them  and  it  was  thought  advisable  to  remove  the  teeth  that 
were  crowned,  as  the  patient  was  confined  to  his  bed  and  it  was  impossible  to 
open  the  teeth  and  treat  the  roots  with  any  degree  of  satisfaction.  "Within 
five  weeks  after  the  extraction  the  patient  was  able  to  walk  around,  being  free 
from  all  pain,  and  the  swelling  had  disappeared. 

Case  3 

Confined  to  his  bed  with  arthritis  of  the  knees  and  ankles.  Eemoved 
the  left  superior  first  molar,  it  having  a  slight  infection  above  it;  also 
removed  a  badly  broken-down  root  which  was  the  source  of  some  infection. 
Patient  began  to  improve  within  forty-eight  hours. 

Relatively  small  areas  of  rarefaction  on  the  roots  of  teeth  con- 
sequent upon  chronic  peridental  infection  are  frequently  the 
cause  of  severe  joint  infection.  In  some  cases  one  single  slight 
area  of  infection,  upon  its  elimination,  has  brought  about  re- 
covery of  the  case. 

Hartzell  and  Henrici0  report  that  in  the  study  of  a  series  of 
seventeen  cases  of  arthritis  deformans  over  one-half  of  these 
patients  showed  improvement,  which  in  a  few  cases  was  pro- 

"Hartzell,  Thomas  B.,  and  Henrici,  Arthur  T. :  A  Study  of  Streptococci  from  Pyor- 
rhea Alveolaris   and   from   Apical   Abscesses,   Jour.    Am.   Med.    Assn,   xliv,    No.    13. 


MOUTH    [NFECTIONS    WD   SYSTEMIC    DISEASE 


.».,.» 


nounced;  other  eases,  however,  became  worse  under  treatment. 
In  a  series  of  seven  eases  of  endocarditis,  in  two  of  the  patients 
the  heart  condition  was  vastly  improved.  Other  systemic  dis- 
turbances studied  by  them  were  three  eases  of  pernicious  anemia, 
five  cases  of  gastric  ulcer,  and  nine  eases  of  active  arthritis.  In 
the  pernicious  anemia  eases  no  definite  report  was  made  by  the 
investigators,  although  they  state  that  one  man  showed  a  marked 
progressive  increase  in  the  blood  count  after  removal  of  some 
of  the  abscessed  teeth,  but  that  he  left  the  hospital  before  his 
dental  work  was  completed,  and  returned  later  with  a  low  blood 
count.  The  gastric  ulcer  patients,  two  of  whom  had  been  affected 
twelve  to  fourteen  years  with  frequent  recurrences  in  that  time, 


Fig.  436. — Case  1. 

had  no  recurrence,  since  eliminating  the  mouth  infections,  dur- 
ing a  period  of  observation  of  two  years  and  five  months  after 
the  dental  work  was  completed.  The  arthritis  patients  all  showed 
a  marked  improvement  beginning  in  some  cases  a  few  hours 
after  removing  the  abscessed  teeth. 

The  following  reports  of  cases  studied  by  the  author  from  a 
series  of  several  hundred  will  throw  some  light  on  the  role  of 
mouth  infections  as  sources  of  systemic  intoxications. 

Case  1   (Fig.  436) 
Woman,  aged  thirty-six,  had  previously  been  in  apparent  good  health  but 
complained  of  severe  pain  in  her  face.  In  addition,  she  complained  of  a  series 
of  symptoms  typical  of  general  toxemia.     She  seemed   anemic  and   decidedly 


556 


DENTAL   PATHOLOGY 


below  par.  She  sought  the  services  of  a  dentist  for  the  purpose  of  ascertain- 
ing whether  any  abnormality  could  be  detected  in  her  teeth  that  would  ac- 
count for  the  reflex  pain  from  which  she  had  been  suffering  for  some  time  past. 
An  area  of  rarefying  osteitis  was  found  around  the  root  of  the  second  lower 
bicuspid,  indicative  of  chronic  sepsis  in  the  peridental  tissues  and  within  the 
bony  structures.  The  tooth  had  been  previously  treated  and  the  root  canal 
carefully  filled.  The  bicuspid  was  extracted  and  almost  immediately  the  pain 
and  toxic  symptoms  began  to  improve,  and  have  continued  so  uninterruptedly 
ever  since. 

Case  2  (Fig.  437) 
Man  aged  forty-five  gave  a  history  of  continued  good  health  up  to  the  time 
of  the  incidence  of  the  symptoms  which  led  to  his  being  placed  under  our 
observation.  He  had  evidently  been  a  man  of  vigorous  constitution  and  non- 
sedentary  in  his  habits.  He  complained  of  loss  of  appetite,  lassitude,  and  an 
inability  to  exert  himself  to  any  extent  without  experiencing  a  sense  of  fatigue. 


Fig.  437. — Case 


Tlic  radiogram  (Fig.  437)  showed  a  marked  chronic  septic  condition  under  the 
roots  of  the  lower  second  molar,  which  evidently  had  been  treated  years  pre- 
viously and  in  which  the  root  canal  had  not  been  completely  filled.  There  was  a 
tenderness  to  percussion  in  several  teeth  and  consequently  a  definite  diagnosis 
could  not  lie  made  at  the  time.  The  radiogram  came  to  our  assistance,  the 
offending  tooth  was  extracted,  and  a  complete  recovery  followed  within  a 
period  of  three  or  four  weeks. 

Case  3  (Fig.  438) 

Man,  aged  about  sixty  years.    This  case  seems  to  us  to  present  features  of 

special   interest    because  the   septic,  conditions  about  the  roots  of  some  of  the 

teeth  were  evidently  responsible  for  an  interruption  in  the  mental  balance  of 

the  patient.     The  man,  of  limited  means,  had  endeavored  for  some  time  past 


MOUTH    [NFECTIONS    AND   SYSTEMIC    DIS]   \>l. 


557 


to  secure  a  berth  in  an  old  man'-  home,  bul  on  accounl  of  the  mental  and 
physical  symptoms  the  authorities  of  the  institution  rejected  his  application. 
He  was  referred  by  bis  physician  to  ascertain  whether  any  abnormality  could 
exist  in  his  jaws  ami  around  his  teeth  which  could  be  made  to  accounl  for 
the  toxic  symptoms  from  which  he  was  suffering  and  also  for  the  disturbance 
in  psychic  function.  We  found  that  which  would  warrant  one  in  assuming 
thai  the  foci  of  infection  in  his  jaws  were  at  leasl  a  factor  in  the  production 
of  the  pathologic  symptoms  herein  described.  On  the  left  side  conditions 
were  as  follows : 

A  chronic  abscess  around  the  roots  of  the  lower  fust  bicuspid;  an  incar- 
cerated root  in  the  upper  jaw  mesial  to  the  second  molar;  also  foci  of  in- 
fection in  tin-  distal  root  of  the  lower  third  molar,  above  ami  around  the 
loots  of  the  upper  second  bicuspid  and  upper  third  molar.     On  the  right  Bide 


Fig.    438.— Case   3.      A,    left;    B,    right. 


a  number  of  foci  of  infection  could  be  detected  in  the  lower  and  upper  jaws. 
All  the  teeth  that  were  considered  responsible  for  the  conditions  herein 
described  were  extracted  and  the  improvement  that  followed  was  so  marked 
that  he  was  permitted  to  become  a  member  of  the  household  in  the  institu- 
tion for  the  aged,  to  which  admission  had  been  denied  him  some  months  pre- 
viously. 

Case  i  (Fig.  439) 
Woman,  aged  about  thirty,  gave  a  history  of  rheumatoid  arthritis  with 
marked  pain  in  the  region  of  the  shoulder  blades;  pseudoankylosis ;  marked 
anemia,  fatigue,  lassitude,  etc.  This  case  also  exhibited  marked  reflex  nervous 
manifestations.  From  this  case  Streptococcus  viridans  was  isolated.  The  tooth 
that  was  considered  beyond  therapeutic  measures  (the  lower  left  second  molar) 


558 


DENTAL    PATHOLOGY 


was  extracted;  some  of  the  other  teeth,  the  seat  of  chronic  septic  inflamma- 
tions, were  treated  in  the  approved  ways,  while  the  a  piers  of  the  single 
rooted  teeth  were  amputated.  The  improvement  which  has  followed  is 
most  encouraging. 


Fig.    439.— Case    4. 


Fig.   -140.— Case   5. 


Case  5  (Fig.  440) 

Man,  aged  fifty  years,  complained  of  pain  in  the  shoulder  on  the  same 
side  as  that  upon  which  was  found  to  exist  a  chronic  septic  focus  around  the 
apical  third  of  a  lower  bicuspid  tooth.  Removal  of  the  tooth  was  followed 
by  complete  recovery. 


MOUTH   INFECTIONS   AND   SYSTEMIC   DISEASE 


559 


Case  6 
Woman,  aged  aboul  forty,  gave  a  history  of  no  pain,  bul  on  the  other 
hand,  one  of  disturbance  of  nutrition,  accompanied  by  anemia.  Being  the 
wife  of  a  physician,  her  case  was  studied  with  particular  care  by  a  number 
of  medical  practitioners,  all  of  whom  reported  absence  of  viscera]  Lesion. 
Several  foci  of  infection  were  found  in  the  mouth,  namely,  one  around  the 
roots   of   the   lower   first   bicuspid,   one   around    the   roots   of   the   lower   right 

sec 1  molar,  and  one  on  the  distal  side  of  the  upper  right  second  bicuspid. 

Eradication   of  these  anas  was  followed  by  decided  improvement. 

Case  7 

Woman,  aged  thirty  years.  This  patient  exhibited  symptoms  of  intense  gen- 
eral toxemia  for  a  number  of  months.  Prior  to  the  onset  of  these  symptoms  she 
reported  having  been  in  good  health.  She  was  referred  to  us  to  ascertain 
whether  the  condition  of  the   lower  first   molar,  which  had  been   treated   and 


Fig.  441.— Case  7. 


the  root  canals  filled,  was  satisfactory.  Suspicion  had  been  aroused  because 
the  tooth  was  slightly  tender  to  percussion.  While  a  slight  infection  was 
present  in  this  tooth,  the  main  difficulty  was,  however,  in  the  second  bicuspid 
(Fig.  441).  This  patient  was  in  such  an  exhausted  condition  as  to  require 
anywhere  from  sixteen  to  twenty-four  hours  of  sleep  a  day,  and  even  after 
such  a  long  period  of  quietness  she  would  awake  with  a  feeling  of  fatigue  as 
intense  as  it  seemed  to  be  at  the  time  of  retiring.  The  lower  second  bicuspid 
was  extracted,  and  in  the  course  of  a  few  weeks  the  symptoms  entirely  dis- 
appeared. She  has  since  reported  that  eight  hours  of  sleep  satisfy  her  com- 
pletely. 

Case  8   (Fig.  442) 

Man,  aged  about  forty-five,  gave  a  history  of  lameness  in  the  right  shoul- 
der, torticollis,  and  a  continued  toxic  condition.     He  did  not  have  to  state 


5G0 


DENTAL    PATHOLOGY 


that  he  was  a  sick  man — it  was  self-evident.  The  roots  of  the  first  molar 
showed  an  intensified  septic  process.  The  tooth  was  extracted,  and  there 
followed  in  due  time  a  marked  improvement. 


Fig.  442.— Case  8. 


Fig.  443.— Case  9. 


Case  9   (Fig.  443) 
Man,  aged  about  forty-five  years,  had  symptoms  of  toxin  absorption  and 
slight  pain  on  the  left  side  of  the  mandible.     A  large  septic  focus  was  found 
between  and  below  the   roots  of   the   lower  first  molar.     Extraction  was  fol- 
lowed by  recovery. 


MOUTH    [NFECTIONS    AND   SYSTEMIC    DISEASE  .",111 

In  a  series  of  three  hundred  eases  of  gastrointestinal  lesions, 
50%  per  cent,  or  about  L52  patients,  had  mouths  in  which  l'<<cal 
infections  were  present.  Nineteen  ou1  of  twenty  patients  suf- 
fering from  ulcers  were  found  also  to  be  sufferers  from  pyorrhea.7 

Mouth  infection  is  probably  a  predisposing  cause  of  cancer. 
In  those  cases  a  chronic  infection  of  the  alimentary  tract  is  pro- 
duced and  maintained  by  the  infectious  oral  conditions,  the  gas- 
trointestinal infection  acting  as  the  irritant  which  brings  about 
the  proliferation   of  the  cancer  eells. 

In  t lie  prevention  and  treatment  of  tuberculosis  it  is  of  primary 
importance  to  eliminate,  so  far  as  possible,  any  additional  sources 
of  infection  in  order  that  the  patient  should  not  he  subjected  to 
the  additional  drain  on  his  vitality  by  the  subconscious  effort  to 
ward  off  infections  additional  to  the  chronic  one  from  which  he 
suffers.  It  is  for  this  reason  that  physicians  with  the  proper  con- 
ception of  the  etiology,  pathology,  and  treatment  of  tuberculosis, 
endeavor  to  not  only  treat  the  specific  infection,  but  coincident 
therewith  aim  at  the  eradication  of  all  other  sources  of  chronic 
infection — of  course  herein  including  infections  in  and  about  the 
teeth.  Chronic  infections  of  the  gingivae  and  gums,  chronic  ab- 
scesses on  the  roots  of  teeth,  and  chronic  infections  in  the  tonsils 
and  surrounding  structures,  must  be  eliminated  if  any  degree  of 
success  is  to  be  attained  from  the  measures  instituted  to  arrest 
the  tuberculous  process.  It  is  also  very  probable  that  the  lesions 
above  mentioned  are  instrumental  in  the  incidence  of  tuberculosis, 
and  therefore  in  the  battle  of  prevention  and  cure  every  effort 
should  be  made  to  ascertain  whether  chronic  foci  of  infection  are 
present  anywhere  in  the  body,  and  if  present,  no  compromise 
should  be  reached  other  than  their  complete  eradication. 
AVhether  the  oral  foci  of  infection  are  directly  instrumental  in 
inciting  the  lesion,  or  whether  indirectly,  by  lowering  the  vital 
resistance  of  the  individual,  it  matters  not,  to  any  extent,  so  far 
as  the  ultimate  purpose  of  treatment  is  concerned ;  in  either  case 
all  untoward  conditions  should  be  eradicated,  since  they  are  di- 
rectly and  indirectly  constant  sources  of  danger  to  those  in  whose 
mouths  thev  are  located. 


7Read,   J.    Marion.:      Jour.    California    State   Dental   Association. 


562  DENTAL    PATHOLOGY 

Secondary  Focal  Infections 

In  the  course  of  observations  on  the  relationship  of  focal  in- 
fections to  systemic  disease  we  are  frequently  confronted  with 
a  problem  of  difficult  solution:  viz.,  can  it  be  established  without 
more  than  reasonable  doubt  that  the  chronic  denial  lesion  is  di- 
rectly responsible  for  the  onset  of  the  systemic  involvement  of 
which  the  patienl  may  at  the  time  be  the  sufferer,  and  is  it  a 
somatic  involvement  .'  The  general  practitioner  has  only  one  way 
of  reaching  conclusions,  and  that  is  on  the  basis  of  the  clinical 
results  which  follow  his  dental  interventions.  If  after  a  reasona- 
ble period  of  time  the  anticipated  improvements  do  not  material- 
ize, then  ipso  facto  he  concludes  that  the  diagnosis  of  the  etiology 
of  the  general  disease  was  erroneous:  on  the  other  hand,  if  the 
patient  shows  improvement,  the  chronic  infections  in  and  around 
the  teeth  must  have  been  the  sources  of  infection  of  the  lesions 
in  the  circulatory  system,  gastrointestinal,  respiratory,  or  genito- 
urinary tracts,  or  in  articulations,  muscles,  nerves,  or  what  not. 

It  is  of  the  greatest  importance  in  the  consideration  of  focal 
infections  to  bear  clearly  in  mind  jl  that  thi  absence  of  im- 
provement, clinically  observable,  does  not  prove  that  the  foci  of 
infection  art  not  etiologic  factors  of  the  disease,  and  (2)  that  the 
amelioration  of  thi  general  symptoms  does  not  prove  that  the  foci 
under  suspicion  an  somatically  related  to  thi  systemic  involvement. 
There  are  other  factors  and  possibilities  which  must  be  carefully 
considered  if  a  more  correct  determination  is  to  be  made  of  the 
relationship  of  focal  infections  to  systemic  disease. 

Among  the  many  sources  of  infectious  metastases  from  the 
head,  the  soft-tissue  chronic  infections  in  connection  with  the 
abnormal  eruption  of  lower  third  molars  is  selected  as  an  illus- 
tration, because  the  eradication  of  such  a  focal  infection,  even 
if  it  is  the  original  source  of  a  systemic  involvement,  is  not  al- 
ways followed  by  the  disappearance  or  even  improvement  of  the 
general  symptoms  to  which  it  may  have  given  rise.  These  so- 
called  third  molar  abscesses  bring  about  the  involvement  of  the 
deep  cervical  lymph  nodes  which,  in  the  event  of  becoming  the 
seat  of  a  chronic  infection,  establish  secondary  foci  of  infection, 
and  not  until  this  new  source  of  absorption  of  bacteria  and  their 
toxins  is  removed  can  the  general  symptoms  improve.  There- 
fore, once  a  focal  infection  in  or  around  the  teeth,  in  the  jaws. 


MOUTH    INFECTIONS   AND   SYSTEMIC   DISEASE  563 

air  sinuses,  or  anywhere  in  the  head,  has  been  discovered,  it 
is  nt'  the  greatesl  importance  to  ascertain  whether  any  secondary 
Eoci  exist,  in  order  that  both  the  primary  and  secondary  infec- 
tions may  be  removed  at  once,  if  at  all  possible  or  practicable. 

Another  example  of  secondary  infections  in  the  head  is  to  be 
found  in  the  maxillary  sinus  as  the  result  of  a  long-  standing 
periapical  infection  in  any  one  of  the  teeth  which  abuts  into 
it.  A  first  molar  may  he  the  seat  of  a  chronic  dentoalveolar  ab- 
scess, suspected  of  being  the  source  of  an  existing  arthritis.  The 
maxillary  sinus  may  or  may  not  appear  clear  on  the  radiogram. 
The  first  molar  is  extracted,  the  floor  of  the  maxillary  sinus  is 
probed  to  ascertain  whether  an  opening  exists  through  the  fun- 
dus of  the  alveolus  or  not.  Then,  in  the  absence  of  this,  the  sinus 
is  declared  healthy,  at  least  in  so  far  as  infection  communicated 
from  that  first  molar  is  concerned.  As  a  matter  of  fact  the 
mucoperiosteum  of  the  sinus  may  be  the  seat  of  a  chronic  in- 
fectious process  from  that  same  molar,  even  in  the  absence  of 
a  macroscopic  opening,  and  may  be  the  seat  of  a  focal  infection 
not  always  detectable  in  a  radiogram.  Therefore,  in  the  case  of 
chronic  abscesses  upon  the  roots  of  such  teeth  as  are  in  proximity 
to  the  maxillary  sinus,  the  condition  of  the  mucoperiosteum  of 
the  sinus  should  be  thoroughly  investigated  both  clinically  and 
radiographically.  Radiograms  examined  by  the  author,  when 
showing  involvement  of  the  maxillary  sinus,  have  in  many  cases 
proved  to  be  unreliable  and  misleading.  If  the  dentist  is  unable 
to  reach  a  conclusion  on  the  basis  of  a  combination  of  clinical 
and  radiographic  examination,  the  services  of  a  specialist  in 
rhinology  should  be  enlisted. 

These  secondary  focal  infections  may  be  located  in  the  head  in 
more  or  less  close  proximity  to  the  dentoalveolar  abscess,  or  in 
areas  of  the  body  at  a  distance  from  the  original  focus,  e.g..  a 
secondary  focus  from  the  original  dental  or  oral  focus  in  the 
gallbladder  or  in  the  appendix. 

From  the  foregoing  we  are  led  to  the  conclusion  that  the 
eradication  of  a  chronic  dentoalveolar  abscess,  or  abscesses  cor- 
rectly suspected  of  being  the  cause  of  some  form  of  systemic  in- 
volvement, will  not  be  followed  necessarily  by  an  improvement 
of  symptoms  until  the  secondary  foci  to  which  they  may  have 
given  rise  are  likewise   eliminated.     Because  the  symptoms  do 


564  DENTAL    PATHOLOGY 

not  improve  is  not  sufficient  evidence  that  the  dental  chronic 
infections,  intraosseous  or  extraosseous,  are  not  primarily  re- 
sponsible for  the  systemic  derangements. 

Concerning  the  somatic  phase  of  focal  infections,  namely,  as 
to  whether  the  infecting  organisms  and  their  toxins  actually 
reach  by  way  of  an  anatomic  route  the  area  in  which  they  mul- 
tiply; or  whether  their  pathologic  significance  is  the  result  of 
additional  stress  placed  upon  the  body  defences,  thereby  de- 
creasing the  chances  for  bacterial  destruction  and  tissue  repair 
in  areas  previously  infected  from  other  sources — one  conclusion 
only  can  be  reached.  The  dental  and  oral  foci,  whether  the  source 
of  somatic  infection,  or  whether  they  act  by  decreasing  the  effi- 
ciency in  numbers  of  the  antibodies  in  the  blood  and  tissues,  must 
be  eliminated.  The  latter  possibility  has  been  conclusively 
proved  under  the  writer's  observation  in  his  many  cases  of  ac- 
tive tuberculosis  and  gastrointestinal  derangements,  which  im- 
proved markedly,  showing  an  arrestment  of  the  tuberculous  proc- 
ess following  the  eradication  of  extraosseous  oral  foci. 


CHAPTER  XLY 

DISEASES  OF  THE  GINGIVA,  GUMS,  AND  ORAL  MUCOUS 

MEMBRANE 

Elsewhere  in  this  work  the  gingivae  and  gums  have  been  studied 
when  in  a  condition  of  health  as  well  as  when  the  seat  of  disease 
processes  which,  by  continuity,  eventually  involve  the  peridental 
membrane  and  alveolar  process.  In  this  chapter  it  is  the  aim 
in  view  to  discuss  those  diseases  of  the  oral  mucous  membrane 
in. which  large  areas  of  tissue,  relatively  speaking,  are  eventually 
involved,  giving  rise  to  a  gingivitis,  a  stomatitis  or  to  a  combina- 
tion of  both  processes.  ( iinuivitis.  we  define,  therefore,  as  an  in- 
flammation, acute  or  chronic,  of  the  gingiva?  or  gums  or  both 
structures;  and  stomatitis,  as  an  inflammation,  acute  or  chronic, 
of  the  mucous  membrane  which  lines  the  floor  of  the  mouth, 
cheeks  or  palate.  Most  forms  of  stomatitis  develop  in  the  period 
from  infancy  to  childhood,  although  in  adults  some  of  the  most 
severe  forms,  accompanied  by  ulceration  and  sloughing  of  tissue 
are  encountered.  The  mucous  membrane  of  the  cheeks,  lips 
and  the  alveolar  process  may  be  involved  in  their  entirety  in 
certain  forms  of  the  disease;  in  others  only  limited  areas  are 
affected.  The  varieties  of  stomatitis  generally  encountered  are 
the  simple,  catarrhal,  aphthous,  mycotic,  ulcerative,  mercurial, 
and  gangrenous. 

Simple  Stomatitis  (Stomatitis  Simplex) 

A  hyperemie  condition  of  the  oral  mucous  membrane,  which  if 
not  corrected  when  it  first  appears,  acquires  the  characteristics 
of  the  catarrhal  form.  The  membrane  is  sensitive,  especially  to 
hot  and  acid  or  pungent  foods.  It  may  develop  in  the  course  of 
the  eruption  of  the  deciduous  or  permanent  teeth,  it  being  asso- 
ciated with  the  gastric  and  intestinal  disturbances  which  are  in 
some  cases  the  accompaniments  of  so-called  pathologic  dentition. 
Fever  may  be  present  when  it  develops  in  children,  and  either 
diarrhea  or  constipation  accompanies  it.  In  adults  the  ingestion 
of  highly  spiced  foods  and  intemperance  in  the  use  of  tobacco 

565 


566  DENTAL   PATHOLOGY 

and  alcohol  are  some  of  the  etiologic  factors  of  this  form  of 
stomatitis.  The  disease  may  last  from  a  few  hours  to  a  few  days, 
but  subsides  shortly  after  the  elimination  of  the  cause. 

Pathologic  Anatomy. — The  characteristic  feature  of  the  disease 
is  the  dilatation  of  the  blood  vessels  of  the  connective-tissue  mat 
of  the  mucous  membrane,  the  result  of  the  presence  in  the  mouth 
of  some  form  of  irritation,  which,  if  not  eliminated,  decreases  the 
vital  resistance  of  the  tissues  and  prepares  the  field  for  subse- 
quent bacterial  infection.  Areas  of  elevated  mucous  membrane 
may  be  distributed  throughout  the  mouth.  It  should  be  borne 
in  mind  that  a  simple  stomatitis  is  the  antecedent  of  the  catar- 
rhal (infectious)  form,  and  that  from  its  etiology  bacterial  irrita- 
tion is  excluded.  Therefore,  in  addition  to  the  etiologic  factors 
already  mentioned,  must  be  added  the  irritation  caused  by  de- 
fective partial  or  full  plates,  concentrated  germicidal  solutions 
used  as  mouth  washes,  and  salivary  deposits  impinging  upon  the 
gum  tissues.  While  not  in  line  with  the  aims  of  this  book  to 
enter  into  therapeutic  discussions,  it  may  nevertheless  be  ad- 
visable to  suggest  a  general  line  of  treatment  which  in  the  case 
of  simple  stomatitis  should  be  undertaken  as  soon  as  the  first 
symptoms  of  the  disease  appear.  All  sources  of  irritation,  me- 
chanical or  chemical,  should  be  at  once  eliminated,  and  the  teeth 
should  be  subjected  to  a  thorough  scaling  and  polishing.  An 
antiseptic  mouth  wash  should  be  prescribed,  either  a  light  purple 
potassium  permanganate  solution  (1:3500),  or  a  potassium  chlo- 
rate solution  2:100. 

Catarrhal  Stomatitis 

Any  one  of  the  etiologic  factors  mentioned  in  connection  with 
the  simple  form  of  stomatitis,  when  permitted  to  persist,  or  a  com- 
bination of  two  or  more  of  these  etiologic  factors  plus  bacterial 
infection,  are  responsible  for  the   onset  of  catarrhal  stomatitis. 

There  is,  besides  redness  of  the  mucous  membrane  of  the  palate, 
floor  of  the  mouth,  cheeks  and  gums,  all  of  the  symptoms  and 
manifestations  of  a  well-established  infectious  inflammation. 
There  will  be  swelling,  rise  in  temperature  from  one  to  four  de- 
grees, pain  upon  mastication,  increased  flow  of  saliva,  spongy 
texture  of  the  gums-,  increased  sensitiveness  of  the  mucous  mem- 
branes at  all  times,  even  to  the  point  of  making  mastication  im- 


,;i\.;i\   E,    GUMS    AND   ORAL    MUCOUS    MEMBRANE  567 

possible,  fetidity  of  the  breath;  in  some  cases  instead  of  an 
increased  How  of  saliva,  the  mouth  will  feel  dry  and  ho1  and  an 
abundance  of  thick  and  stringy  mucus  will  be  present.  This 
form  is  generally  associated  with  disturbances  of  digestion  and 
whether  il  occurs  in  children  or  adults,  aegled  of  the  teeth  and 
investing  tissues  is  the  paramount  etiologic  factor.  Chronic  dis- 
orders such  as  tuberculosis,  syphilis,  diabetes  may  acl  as  predis- 
posing causes  by  reason  of  the  lessened  resistance  of  individuals 

so  affected. 

Pathologic  Anatomy.— A  marked  congestion  of  the  mucous 
membrane  and  an  excessive  mucus  discharge  are  the  salienl 
phenomena  in  this  form  of  •  stomatitis.  Epithelial  desquamation 
and  edema  are  present,  Mucoid  degeneration  of  the  superficial 
epithelium  and  of  the  alveolo-tubular  glands  occurs.  If  many 
polymorphonuclear  leucocytes  in  various  stages  of  degeneration 
are  present,  the  discharge  assumes  a  whitish  or  yellowish  color. 
Following  the  elimination  of  the  cause  or  group  of  causes,  a  re- 
generation of  the  lost  superficial  epithelium  occurs  and  the  mu- 
cous membrane  again  resumes  its  normal  color  and  texture. 
Catarrhal  stomatitis  is  frequently  an  accompaniment  of  scarlet 
fever,  measles,  smallpox,  and  typhoid  fever. 

Ulcerative  Stomatitis  (Fig.  444) 

Ulcerative  stomatitis  is  an  intense  inflammation  of  the  mucous 
membrane,  accompanied  by  ulceration  and  destruction  of  soft 
tissue  by  gangrenous  decomposition. 

In  ulcerative  stomatitis  the  systemic  factor  plays  an  important 
part.  It  does  not  occur  unless  the  vitality  is  greatly  reduced  by 
some  general  disease.  It  may  follow  the  continued  administra- 
tion of  mercury,  especially  if  the  teeth  and  the  mouth,  as  a  whole, 
were  not  placed  in  good  condition  before  the  treatment  was  be- 
gun. The  neglect  of  the  hygiene  of  the  mouth  through  insuffi- 
cient brushing,  the  presence  of  salivary  and  subgingival  deposits, 
excessive  smoking  and  drinking,  or  in  children's  diseases  of 
nutrition,  the  exanthemata,  etc.,  are  factors  of  importance  in  the 
etiology  of  the  disease. 

The  ulcers  in  ulcerative  stomatitis  start  upon  the  gingival  tis- 
sues as  a  rule,  although  they  may  be  located  upon  any  part  of 
the  mouth,  the  buccal  or  palatal  mucous  membranes,  the  floor  of 


568  DENTAL    TATIIOLOGY 

the  mouth  and  upon  the  tongue.  The  affected  gingival  margin 
shows  a  dark  yellow  or  greenish  appearance.  Ulcerative  stoma- 
titis is  contagious  and  frequently  spreads  to  members  of  a 
family,  and  it  assumes  epidemic  form  among  soldiers,  in  factories, 
and  wherever  large  bodies  of  men  congregate. 

The  disease  is  not  strictly  local.  General  symptoms  character- 
istic of  toxemia  are  frequently  present.  There  may  be  intestinal 
symptoms,  viz.,  lack  of  appetite,  rise  in  temperature,  and  profound 
depression.  The  gangrenous  decomposition  of  the  ulcerated  areas 
gives  off  a  very  offensive  odor  and  the  tissues  of  the  mouth  be- 
come so  painful  as  to  render  impossible  the  mastication  of  food. 
The  infection  may  spread  to  the  periosteum,  causing  destruction 
of  the  alveolar  process  and  the  loosening  of  the  teeth,  especially 
in  young  children. 

It  develops  occasionally  in  the  course  of  pyorrhea  alveolaris 
following  an  exacerbation  of  the  otherwise  chronic  infection 
characteristic  of  that  disease.  Among  the  chief  etiologic  factors, 
must  be  mentioned  neglecting  the  teeth,  the  presence  of  cavities, 
and  sharp  edges  of  fillings,  crown,  etc. 

A  suggestion  as  to  treatment  may  not  be  out  of  place.  It 
should  consist  of  local  and  systemic  measures.  The  local  measures 
should  include  the  following  steps: 

1.  Thorough  scaling  and  polishing  of  the  teeth. 

2.  Temporary  fillings  where  needed. 

3.  10  to  20  per  cent  silver  nitrate  applied  to  the  ulcerated  tis- 
sues, or  a  10  per  cent  glycerinated  salvarsan,  or  liquor  potassii 
arsenitis. 

-4.  Frequent  irrigations  of  the  mouth  with  potassium  perman- 
ganate solutions  of  proper  strength  (1:3500). 
The  systemic  treatment  should  include  : 

1.  Rest,  nonirritating  diet,  abstinence  from  tobacco  and  alcohol. 

2.  Laxatives  to  insure  complete  elimination. 

3.  Administration  internally  of  potassium  chlorate,  1  teaspoon- 
full  every  three  hours,  of  a  solution  of  24  grains  to  the  ounce. 
For  children  reduce  the  dose  to  12  grains  to  the  ounce. 

Pathologic  Anatomy. — The  anatomic  lesion  in  ulcerative  stoma- 
titis results  from  the  infection  of  any  portion  of  the  gingival 
mucous  membrane  by  several  organisms,  especially  staphylococci, 
streptococci,  the  Bacillus  fusiform  is  and  the  spirilla  of  Vincent. 


Fig     444 —Ulcerative   stomatitis.      (After    Preiswerk.) 


GINGIVA,   GUMS    AND   ORAL    MUCOUS    MEMBRANE 


569 


The  gingival  margins  are  the  usual  local  ions  for  the  beginning 
0f  tne  infection  and  may  involve  the  gingivae  over  only  a  few 
teeth,  or  in  extreme  cases,  the  entire  gingivae  may  he  affected. 
The  tissues  show  evidences  of  gangrenous  decomposition  which 
follows  the  destruction  of  life  in  the  tissues  by  bacterial  activity. 
Tn  rare  cases  the  gums  remain  unaffected,  the  buccal  and  palatal 
mucous  membrane  being  then  the  tissues  involved.  The  gingiva?, 
when  it  is  the  seat  of  the  infection,  appears  covered  with  a  yel- 
lowish fibropurulent  exudate.  The  inflammatory  process  is  not 
limited  to  the  area  immediately  adjacent  to  the  tissues  undergo- 
ing gangrene,  but  the  entire  mucous  membrane  may  appear 
deeply  inflamed.  High  temperature,  loss  of  appetite,  mental  de- 
pression, and  extreme  fetidity  of  the  breath,  are  the  accompany- 
ing symptoms. 

Mercurial  Stomatitis 

Mercurial  ptyalism— mercurial  salivation— is  an  infection  of  the 
mucous  membrane  of  the  mouth,  following  decrease  in  resistance 
against  infection  brought  about  by  the  irritating  effects  of  mer- 
cury and  its  compounds  when  administered  for  a  prolonged  period 
in  the  treatment  of  syphilis.    The  salts  of  mercury  are  eliminated 
in  part  by  the  saliva,  and  when  their  use  has  been  constant  for 
months,  the  mucous  membrane   is  constantly  and  continuously 
subjected  to  the  irritating  action  of  these  compounds.     The  first 
symptoms  of  mercurial  ptyalism  consist  in  redness  of  the  mucous 
membrane,  offensive  breath,  a  generalized  pericementitis  over  all 
the  teeth,  and  an  increase  in  the  flow  of  saliva.    If  the  administra- 
tion of  mercury  is  not  discontinued,  the  gums  ulcerate,  and  the 
peridental  membranes  become  so  vTeak  and  relaxed  that  the  teeth 
appear  to  be  ready  to  drop  out.    The  infection  spreads  from  the 
peridental  membrane  to  the  alveolar  process,  and  in  severe  cases 
exfoliation  of  sequestra  takes  place.    The  tongue  may  be  swollen 
and  the  seat  of  ulcerations,  and  the  salivary  glands,  especially  the 
parotid,  may  become  swollen  and  inflamed.     The  symptoms  of 
ptyalism  set  in  relatively  early  during  the  administration  of  mer- 
cury if  the  mouth  has  been  neglected,  i.e.,  in  the  presence  of  cavities, 
infections  of  the  peridental  membrane,  salivary  and  subgingival 
deposits,  broken-down  crowns  and  teeth.    It  also  develops  among 
workmen  in  the  industries  in  which  mercury  is  employed.     The 
infection  is  polymicrobic  in  character. 


570  DENTAL    PATHOLOGY 

Aphthae — Canker  Sores — and  Aphthous   Stomatitis 

Individual  aphthae,  or  canker  sores,  are  localized  disturbances 
of  the  oral  mucous  membrane,  the  manifestations  of  some  form 
of  mild  irritation.  An  aphtha  is  a  small  rounded  vesicle,  white 
or  gray  in  color,  which  begins  as  a  hyperemic  spot  and  subse- 
quently, because  of  degeneration  of  the  superficial  epithelium,  with 
a  fibrinous  exudate,  assumes  the  appearance  of  a  white  or  grayish 
vesicle.  The  vesicle  in  a  few  days  collapses  or  breaks  down,  ex- 
posing an  ulcerated  understructure.  At  the  beginning  of  the 
eruption  the  hyperemic  spots  are  sensitive  to  sour  or  sweet  food- 
stuffs, the  patient's  attention  being  first  called  to  their  existence 
by  their  sensitiveness.  One  or  a  number  of  aphthae  may  develop 
in  one  or  several  areas  of  the  mucous  membrane,  such  as  on 
each  side  of  the  frenum  of  the  tongue,  on  the  margin  of  the 
tongue,  on  the  internal  surface  of  the  lips,  especially  on  the 
lower;  rarely  on  the  internal  surface  of  the  upper  lip  or  upon 
the  gums.  The  symptoms  to  which  the  aphtha?  give  rise  are  very 
light,  and  in  a  few  days  the  disorder  disappears. 

Aphthous  stomatitis,  or  an  inflammation  of  the  oral  mucous 
membrane,  accompanied  by  the  formation  of  vesicles  or  aphthae 
which  may  join  or  coalesce,  each  surrounded  by  a  reddish  mucous 
membrane,  develops  in  poorly  nourished  infants  and  children  in 
connection  with  the  eruption  of  the  teeth,  or  following  such  ex- 
haustive diseases  as  whooping  cough  or  bronchopneumonia.  In 
adults  it  may  develop  in  pregnant  women. 

Pathologic  Anatomy. — It  is  not  uncommon  to  find  in  the  litera- 
ture that  aphthous  stomatitis  and  thrush  are  described  as  iden- 
tical diseases  and  of  identical  pathogenicity.  This  is  indeed  a 
mistake,  as  the  disease  under  consideration  is  not  the  manifesta- 
tion of  a  mycotic  infection,  but  a  probable  superficial  infection 
by  any  one  of  a  number,  or  combinations,  of  mouth  organisms. 
Hyperemic  spots  here  and  there,  areas  of  congestion,  stagnation 
and  consequent  decreased  tissue  resistance  and  subsequent  in- 
fection, fibrinous  effusions,  degenerated  and  dead  epithelium  in 
the  vesicular  formations — summarize  the  pathologic  features  of  the 
disease. 


GINGIV/E,    GUMS    AND   ORAL    MUCOUS    MEMBRANE  571 

Thrush 

Thrush  is  an  infection  of  the  mucous  membrane  of  the  mouth 
caused  by  the  saccharomyces  albicans  (oidinm  albicans)  which  de- 
velops in  athreptic  infants  and  weakened  adults.  It  is  charac- 
terized at  the  beginning  by  extreme  dryness  of  the  month  (partial 
arrestment  of  salivary  secretion)  and  an  annoying  sensation  of 
intense  heat.  The  tissues  of  the  mouth  become  red  and  the  tongue 
papilla?  project  above  the  surface.  The  patches  themselves  may  be 
small,  or  they  may  coalesce,  covering  the  area  in  which  they  are 
located  with  a  whitish  deposit.  On  account  of  the  abundance  of 
a  white  discharge  of  a  fibrinous  nature,  or  wherever  the  sac- 
charomyces is  active  and  multiplying,  the  name  of  creamy  stoma- 
titis has  been  given  to  this  form  of  stomatitis  by  French  writers. 
It  is  by  this  name  that  stomatite  cremeuse  is  described  in  the  older 
and  in  some  of  the  recent  French  textbooks.  The  patches  may 
develop  on  any  portion  of  the  tongue,  lips,  cheeks,  floor  of  the 
mouth,  palate,  hard  or  soft,  perhaps  on  the  gums  and  even  in  the 
throat  or  pharynx.  The  patches,  at  first  white,  later  assume  a  dark 
color.  Frey1  has  observed  many  cases  of  the  disease,  and  from 
the  original  in  French  we  quote  as  folloAvs:  "The  systemic  in- 
volvement varies  according  to  the  patient's  age.  In  the  new- 
born there  may  be  difficulty  in  nursing  and  deglutition,  diarrhea, 
vomiting;  in  the  adult  the  sensation  of  dryness  is  very  marked. 
In  the  aged,  especially  those  affected  with  chronic  disorders  of 
the  urinary  tract  intense  dysphagia  is  present,  especially  in  con- 
nection with  the  ingestion  of  food  requiring  mastication  and  in- 
salivation.  Two  forms  are  observable  in  children,  one  in  well 
nourished  infants  simultaneous  with  the  presence  of  colic,  diar- 
rhea and  vomiting  of  short  duration  and  another  form  in  poorly 
nourished  infants  suffering  from  persistent  diarrhea,  vomiting, 
abdominal  tympanitis  and  all  other  manifestations  of  serious  di- 
gestive disturbances." 

The  acid  fermentation  of  milk  and  starches  in  the  mouth  is 
closely  associated  with  the  development  of  thrush,  as  the  sac- 
charomyces albicans  finds  in  that  kind  of  medium  a  soil  favorable 
for  its  growth  and  development.  It  should  be  remembered,  how- 
ever, that  while  decided  alkalinity  arrests  the  growth  of  the  sac- 


U'athologie  de  la  Bouche  et  des  Dents. 


572  DENTAL    PATHOLOGY 

charomyces,   it   may   continue   to   grow   in   a   mildly  alkaline   or 
neutral  medium. 

Pathologic  Anatomy. — The  stratified  squamous  epithelium  of 
the  mucous  membrane  becomes  the  seat  of  a  fibrinous  inflamma- 
tion, brought  about  by  the  growth  and  development  within  it- 
self of  the  saccharomyces  (oidium)  albicans.  Degeneration  and 
loss  of  superficial  epithelium  occurs,  and  the  infection  may  spread 
into  the  underlying  connective  tissue.  The  membranous  charac- 
ter of  the  patches  is  the  result  of  the  fibrinous  type  of  inflamma- 
tion to  which  the  organism  gives  rise. 

Herpes  Labialis 

Herpes  labialis  (lip  herpes)  is  a  circulatory  disturbance  over 
limited  areas  of  the  lips  caused  by  deranged  nervous  function. 
They  have  the  appearance  of  blisters.  The  epithelium  is  raised 
and  if  scraped  off  or  when  it  sloughs  off,  it  exposes  an  irritated 
connective-tissue  understructure  painful  to  the  touch  and  bleed- 
ing readily.  These  are  also  known  as  cold  sores,  fever  sores  or 
fever  blisters.  The  decreased  or  arrested  secretion  of  the  epi- 
thelial glands  of  the  mucous  membrane  of  the  lips  deprives  the 
lips  of  necessary  lubrication  and  protection  against  air  and  dust 
particles  with  a  consequent  irritation  to  the  nerve  endings,  re- 
sulting in  the  canker  sore  or  fever  blister.  These  sores  occur  upon 
the  lip  during  or  following  colds,  fevers,  typhoid,  or  the  use  of 
the  rubber-dam  for  prolonged  sittings.  The  tissues  of  the  lips 
become  abnormally  dry  and  crack  open  on  the  slightest  provoca- 
tion. 

Affections  of  the  Tongue 

The  tongue  may  be  the  seat  of  deformities  which  interfere  with 
speech.  This  is  due  to  a  short  frenum  which  prevents  the  tongue 
from  being  protruded  in  the  act  of  speaking.  The  tongue  may 
have  a  deep  median  fissure — a  cleft.  The  complete  absence  of 
the  tongue  has  also  been  reported. 

Ulcers  of  the  Tongue 

Simple  ulcers  of  the  tongue  are  usually  the  result  of  irritation 
by  a  jagged  tooth,  crown,  or  some  foreign  body  in  the  mouth. 
They  persist  until  the  irritant  is  removed.     Following  the  de- 


GINGIVAE,    GUMS     \X1>   ORAL    MUCOUS    MEMBRANE  573 

structioD  of  the  superficial  epithelium  they  become  infected,  and 
in  people  pasl  the  age  of  thirty  or  thirty-five  they  should  be 
considered  dangerous,  as  they  are  liable  to  murk  the  beginning 
of  the  development  of  malignant  neoplasms.  In  making  the  diag- 
nosis of  these  ulcers  an  accurate  history  of  their  development 
should  be  secured,  and  if  upon  removing  all  sources  of  irritation 
and  treating  them  with  weak  silver  nitrate  solutions  they  do  not 
disappear  promptly,  the  prognosis  is  serious.  If  there  he  no  in- 
duration the  ulcer  is  probably  a  benign  one,  but  if  induration  be 
present  it  is  probably  a  malignant  one.  Ulcers  of  the  tongue  may 
also  be  syphilitic,  in  which  ease  the  history,  the  presence  of  other 
manifestation  of  syphilis,  and  the  Wassermann  test,  will  determine 
the  diagnosis.  Indurated  ulcers  in  patients  past  forty  years  of  age 
suspected  of  being  carcinomatous,  should  be  excised  without  de- 
lay. 

The  tongue  is  frequently  the  seat  of  inflammatory  disturbances 
brought  about  by  digestive  disorders.  In  these  cases  the  tongue 
appears  red  and  smooth,  the  inflammation  being  as  a  rule  located 
in  the  anterior  portion  of  the  tongue. 

Leucoplakia  of  the  Tongue 

Leucoplakia  is  a  disease  characterized  by  the  presence  upon 
the  dorsum  of  the  tongue  and  mucous  membrane  of  the  mouth, 
particularly  the  buccal,  of  patches  of  a  yellowish  white  color, 
irregular  in  shape,  and  slightly  raised  above  the  mucous  mem- 
brane. They  may  become  indurated,  and  after  the  white  patches 
are  cast  off,  the  under-surface  so  exposed  appears  ulcerated. 
The  superficial  layers  of  the  stratified  squamous  epithelium  are 
thickened,  while  the  deep  layers  exhibit  a  tendency  to  proliferate 
into  the  deeper  structures.  The  patch  may  also  have  a  bluish 
color  and  whenever  it  is  removed,  Avhether  it  be  the  white  patch 
or  the  bluish,  it  leaves  a  raw  surface  behind.  There  is  no  pain 
accompanying  the  patches.  It  may  be  caused  by  the  irritation 
of  tobacco  smoke,  strong  drinks  or  highly  spiced  food,  or  it  may 
be  a  manifestation  of  a  long  standing  syphilis.  Some  authorities 
consider  leucoplakia  as  a  forerunner  of  cancer — a  precancerous 
lesion — and  consequently  insist  upon  the  complete  excision  of  the 
patches,  while  others  believe  that  leucoplakia  is  the  oral  manifes- 
tation of  psoriasis. 


[NDEX 


A 

Abnormalities  of  teeth,  250 

of  upper  lateral  incisor,  267 
Abraded  surfaces,  shape  of,  357 
Abrasion  and  malocclusion,  356 
Abrasion  and   pulp  exposure,  357 
cup-shaped  in  lower  molars,  362 
etiology  of,  356 
from  chewing  gum,  356 
from  gritty   tooth-powders,  356 
from  pipe  and  cigarette  stems,  356 
from  tooth-brush  friction,  356 
in    cuspids,   360 
in    iiicism-s,   358 
of  root,  357 

pathologic  anatomy  of,  357 
pulp  degeneration  in,  358 
tubular   calcification    in,    358 
Abscess,  acute  dentoalveolar,  42-1 

: i  lid  chronic,  difference  in  pathol- 
ogy, 443 
bone  involvement  in,  457 
clinical  symptoms  of,  425 
definition  of,  424 
discharge  from,  424 
discharging  externally,   42!) 
discharging  into  maxillary  sinus. 

427 
discharging     into     nasal     cavity, 

427 
extensive  swelling  from,  431 
involvement  of  face  in,  429 
limited  swelling  from,  431 
most   painful   stage  of,  431 
protrusion  of  tooth  in,  433 
periostitis  in,  435 
chronic    dentoalveolar,    characteris- 
tics   of,    443 
cultures  from,  454 
etiology  of,  436 
fibrous  wall  of,  451 
forms  it  may  assume,  438 
looseness  of  tooth  with,  440 
leucocytes  in  mass  of,  444 
microscopic  anatomy  of,  444 
pathologic  anatomy  of,  436 
sequestrum   formation   in,   468 
sinus  formation  in,  427 
staphylococci  in,  452 
Streptococci  in,  452 
sinuses    from,   436 


Abscess — ('out  M. 

formation,   102 

"hot,"  103 

lateral,    422 

periapical    chronic,    423 

pericemental,   -122 

pyorrheal,    122 

sinusless,  chronic  dentoalveolar,  549 

subacute  dentoalveolor,  430 

chronic    dentoalveolar,    systemic   in- 
volvement   by   bacteria    from, 
551 
Abscesses,  blind,  549 

chronic,    trabeculated,    151 

cold,  103 
Absence  of  teeth,  291 
Acari,  196 
Acarus,  scabiei,  206 
Acid,  dilute,  action  upon  enamel,  219 

effects  of,  on  enamel,  and  perinea 
bility  of,  227 

lactic  in  erosion,  360 
Acidity,   potential,  of  salivary  depres- 
sants, 312 

producers,  .".24 

weak,  in  mouth  washes,  332 
Acroo  dextrin,  322 
Actinomyces   bovis,    181 
Actinomyces  Madura?,   182 
Actinomycosis,  181 
Adamantinoma,    146,   r,:\r, 
A  denocareinomata,  143 
Adenoma,  acimise,  139 

alveolar,   139 

canalicular,  139 

racemose,    139 

simple,  139 

tubular,    139 
Adenomata,  138 
Adhesions,  107 
Age  and  dental  caries,  320 
Age    as   a   predisposing   cause   of   dis- 
ease, 38 
Agenesia,  4  6 

of  enamel,   256 
Agglutinins,  153 
Albumen    in    normal    and    pathologic 

saliva,  371 
Albuminoids,  28 
Alkaloids,    animal,   524 

cadaveric,  413 


57.'. 


576 


INDEX 


Albuminosis,  64 

Albumins,   28 

Alveolar  plate,  exfoliation  of,  462 

process,  atrophy  of,  491 
Alveoli,  cortical  layer  of,    161 

necrosis  of,  462 

rarefying   osteitis   of,   462 
Alveolodental  periosteum,  402 
Ameboid  movement,  32 
Ameloblasts,  245 
Amino-aeids,  27 
Ammonium    carbonate    in    hyperacid 

diathesis,  372 
Amyloid   degeneration,   56 
Anasarca,  95 
Anatomy,  pathologic,  37 

definition  of,  213 
Anemia,  collateral,  82 

local,  82 

neurotic,   82 

idiopathic,  82 

obstructive,   82 
Angina,  Vincent's,  179 
Angioma,   cavernous,   134 
Angiomata,  133 
Angiosarcoma,  126 
Ankylostomiasis,  203 
Anopheles,  188 
Anthrax,  176 
Anthfacosis,  64 
Antibodies,  153 
Antigens,  153 

Antiseptic  power  of  saliva,  315 
Aphthae,  570 
Aphthous  stomatitis,  570 
Apical  areas,  resorption  of,  465 

region,  pyogenic  bacteria  in,  412 
Aplasia,    16 
Arachnida,  196 
Argyria,  64 
Arterioliths,  381 
Arthritis  deformans,  554 
Arthritis  from  oral  foci  of  infection, 

563 
Arthritis,    infectious,     case     histories, 

554 
Arthropoda,  196 
Ascaris  lumbricoides,  200,  201 
Ascites,  96 

chylous,  95 
Ateleiosis,  45 

Atmospheric    pressure,    increased,    ef- 
fects of,  4:'. 
Atrophy,  41 

brown,  46 

combined,  45 

degenerative,  45 

discussion  of,  2.10 

etiology  of,  46 


Atrophy — Cont  'd. 

general,  45 

gross  morbid  anatomy  of,  46 

local,  45 

numerical,  4.1 

pathologic  histology  of,  46 

pathologic  physiology  of,   17 

simple,  4.1 
A  u1  plysis,  76 

B 

Bacillus   acidophilus,   '■'>-  I 

anthracis,  176 

coma,  17(5 

diphtheria,  173 

dysenteric,   175 

fusiformis,  179,  4.12 

gangrense  pulpse,  452 

gingivae  pyogenes,  4.12 

influenza,  178 

pestis,  177 

of  Ducrey,  158 

pulpae  pyogenes,  4.12 

pyoeyaneus,  155 

tuberculosis,  164 

typhosus,  174 
Backward  caries,  328 
Bacteria,  152 

from  chronic  dentoalveolar  abscess, 
.1.11 

higher,  153 

in   dentinal  tubules,  328 

lower,  153 

on  the  number  of,  in  mouth,  315 

putrefactive,   79 

pyogenic  in  apical  region,  412 
Bacterial  absorption  from  subgingival 
space,  380 

enzymes   in   dentin   caries.   326 

infection,    nonreceptivity    to,    214 
Bacteriemia,  114 
Bands  of  Betzius,  221 
Betel-nut  chewing,  383 
Bicuspid,  abrasion  of,   362 

lower  first,  abnormalities  of,  277 

lower  first,  hypoplasia  of,  277 

lower  second,  hypoplasia  of,  277 
Bicuspids,  lower,  with  two  roots,  277 

perfect  fissures  in,  318 

second,  impaction  of,  297 

upper    first,    with    three    cusps    and 
roots,  271 

upper,  hypercementosis  in,  3.11 

upper,  hypoplasia  of,  274 

upper  second,  abnormalities  of,  271 
bifurcation  of  root   of,   273 
with   two    or   three   roots,   274 

upper,  with  three  roots,  273 


INDEX 


577 


Biliary,  calculi,  70 

Blastodermic   layers,   34 

Blastomycetes,    152 

Blastomycosis,   152,  182 

Blind  abscess,  436 

Blood  cells,  solution  of,  by  saliva,  315 

coagulation,    7  1 

excess  of  carbon  dioxide  in,  362,  363 

hemolytic  power  of,  315 

suffusion  of,  'S(i 

supply  of  peridental   membrane,  402 

uric  aeid  suits  in,   196 
Bone   and    eeiiirntmii,    differences   be- 
tween, 233 

cancellated,  455 

changes  in  maxillary  sinus,  427 

compact,  455 

eorpuscles  of,   155 

endochondral,    156 

lamellae  of,  455 

lesions  in  pocket  formation,  .194 

normal    and    pathologic    considera- 
tions, 455 

periosteal,  456 

spongy,   455 
Bright 's  disease,  95 
Bioblasts,  25 
Broncholiths,  70 
Bronchopneumonia,  161 
Bubonic  plague,  177 
Burns,  degrees  of,  42 

C 

Cadaverin,  413,  524 
Caisson  disease,  4.", 
Calcareous  deposits,  381 
in  intestines,  381 
formations  in  pulp  hypertrophy,  53] 
infiltration,  68 
Caleicosis,  64 
Calcification   of   enamel,   direction   of, 

246 
Calcification,  tubular,  in  abrasion,  358 
Calcified   amorphous   bodies   in   defec- 
tive   fissures.    260 
Calcium    acid    phosphate    in    erosion, 

361 
Calculi,  biliary,  70 
renal,  70 
vesical,   70 
Canaliculi  in   cementum,  2::4 
Canals,  Volkmann's,  455 
Cancellated  spaces,  infection  through, 

418 
Cancer  and  mouth  infection,  561 
I  lancer,  colloid,  140 
Candy-makers   mouth,   312 


<  'a  nit  ies,  67 

Canker   sons,   570 

Carbohydrate  diet,  excessive,  manifes- 

tat inn  in  saliva,  37  I 
Carbohydrates,    degrees   of    fermenta- 
tion of,  323 
Carbon   dioxide,   excess   of,   in    blood, 

362 
Carbuncle,  103 
Carcinomata,  139 

basal  cell,  142 

medullary,    1  15 

scirrhous,   143 

simple,  146 
Caries,  among  civilized  races,  311 

aiming  school  boys   and   girls,  313 

ancient  theories  of,  307 

and  age,  320 

and  diet,  311 

and   general   diseases,   .'121 

and  heredity,  321 

and    inflammation    of    gingivae   and 
gums,  320 

and  osteomalacia  of  pregnancy,  320 

and  starchy  foods,  320 

and  sulphocyanates,  371 

and  the  constitutional  factor,  314 

backward,  328 

beginning  of,  334 

chemico-bacterial  theory  of,  314 

chemico-parasitic  theory  of,  310 

coarse  foods  in  relation  to,  312 

conditions  which  favor  progress  of, 
317 

constitutional  factor  in,  414 

dissolution  of  enamel  in,  322 

etiologie  factors  in,  322 

factors  which  favor,  314 

favorable  areas  for,  314 

historical  data,  306 

how  it  advances,  357 

how  limited,  355 

immunity  from,  315 

immunity    to,    in    uncivilized    races, 
311 

in   approximal    surfaces,   predispos- 
ing causes  of,  336 

in  British  races,  313 

in  candy-makers  and  millers,  312 

in  dentin,  progress  of,  342 

in   fissures  and   pits,   33 1 

in  meat-eating   tribes,   312 

in   prehistoric  times,  311 

in  teeth  of  uncivilized  races.  224 

in  the  Maori   rare,  313 

lateral,  326,  328 

malocclusion  and,  319 
Miller's  conclusions  on,  310 


578 


INDEX 


<  laries — Conl  'd. 
of  dentin,  340 

of  dentin,  bacterial  enzymes  in,  320 
onset  of  conditions  which  favor,  320 
pathologic  processes  in,  322 
predisposition     to,     of     hypoplastic 

enamel,  318 
predisposing  causes  of,  .".17,  320 
pulp  infection   in  absence  of,  527 
putrefaction  theory  of,  309 
quantity    of    saliva    in    relation    to, 

316 
races  free  from,  312 
restricted,  320 
role  of  ptyalin  in,  370 
salivary   stimulants    in    relation   to, 

312 
statistics  on,  313 
teeth  in  malocclusion  and,  319 
theories  on,  accepted,   ."'in 
worm  theory  of,  309 

Carious  process  in  dentin,  320 

Cessation,  76 

Catarrhal  stomatitis,   500 

Causes  of  disease,  37 
exciting,   37,    211 
of  hypercementosis,  353 
of  pericemental  inflammation,  sep- 
tic, summary  of  causes,  421 
predisposing,  37,  213 
predisposing,  of  caries,  317 
predisposing,   of  caries   in    approxi- 

mal  surfaces,  32:! 
predisposing,  of  dental  caries,  320 
predisposing,  of  dental  disease,  215 

Cell,    23 

anatomy  of,  24 

chemistry  of,  26 

growth,   32 

nutrition  of,  32 

physics  of,  29 

physiology  of,  32 

staining  reactions  of,  30 

wall,  24 
Cells,  cementoclastic,   250 

giant,  456 

plasma,  451 
Cementoblasts,  233,  407 
Cementoclastic  cells,  250 
Cementum,  233,   248 

and  enamel,  line  of  junction,  228 

canaliculi  of,   234 

caries  of,  349 

changes,    conditions    which    govern, 
250 

chemical  composition  of,  240 

denudation  of,  388 

differences  from  bone,  233 


( 'ementum — Cont  'd. 

fillers  encased  in,  234 

formation  of,  350 

ground  sections  of,  238,  239,  240 

how  deposited,  233 

increases  in   thickness  of,  250 

lacuna1,  233 

lamella;,  233 

increase  in  number  of,  355 
increase  in  size  of,  355 

matrix  of,  234 

nutrition  of,  233 

nutrition  to,  from  dentin,  237 

resorptions  in,  250 
Centrosome,   25 

Cervicolingual  ridge,  abnormalities  of, 
264 

fissured,  265 

hypoplasia  of,  265 
('est  odes,   195,  198 
Chalieosis,  64 
Chancre,  soft,    158 
Chancroid,   158 
Cliemisis,  96 
"Chicken-fat"  clots,  75 
Chicken  pox,  191 
Chilblain,  42 

Chlorides,  increase  of,  in  gouty  diath- 
esis, 372 
Cholera,  Asiatic,  173 
Cholesteatoma,  149 
Cholesterin,  29 
Chorionepithelioma.  149 
Chloroma,  128 
Chondromata,  120 
Chordomata,  121 
Chromatin,  26 
Chronic  gingivitis,  392 
Cilia,  32 

Ciliary  movement,  32 
<  longenital  disease,  40 
Circulatory    activity,    impairment    of, 
215 

changes,  82 
Cleft  palate,  211 
Cloudy  swelling,  48 
Coagulation,  blood,  74 
Coagulation  necrosis,  73 
Coccidiosis,  190 
Calco-globulin,  382 
Cold,  effects  of,  42 
Colloid  degeneration,  52 
Colloids,  29,  30 
Coma  bacillus,  173 
Concretions,  69 
Concussion,  41 
Congestion,  hypostatic,  85 
Conjunctivitis,  epidemic,  179 


[NDEX 


57«J 


Constructive  changes  in  cementum,  250 
Contact,  Lack  of,  379 
Cough,  whooping,  17!) 
Culex,   (mosquito),  188 
Cusp,  lingual,  of  lower  firsl   bicuspid, 
277 
supernumerary  in  upper  first  molar, 
280 
Cuspid,  lower,  supernumerary  root  in, 
273 
hypoplasia  of,  270 
short  rooted,  270 
two  rooted,  270,  272 
radiograph  of,  273 
Cuspids,  abraded,  360 

upper,  abnormalities  of,  269 
longitudinal  section  of,  228 
short  rooted,   270 
Cusps,  three,  in  upper   first  bicuspid, 

271 
Crystalloids,  29,  30 
"Currant   jelly"  clots,   75 
Cylindromata,  147 
Cytoplasm,  23,  25 
Cystic  odontomas,  532 
Cysts,  149 
dental,  532 
dental  or  root,  pathologic  anatomy 

of,  539 
dentigerous,  410,  441 
dermoid,  148 
follicular,  534 
follicular,    pathologic    anatomy    of, 

540 
glandular,   150 
parasitic,  150 
retention,  149 
root,  532 

softening  or  necrotic,  150 
Czermack,  interglobular  spaces  of,  231 

D 

Death,  somatic,  73 

Decalcification,     tardy,    of    deciduous 

teeth,  302 
Deciduous  enamel,  when  it  begins  to 
form,  246 
teeth,  calcification  of,  248 
retention,  291 

tardy  decalcification  of,  302 
Deformities,    macroscopic,    of    central 
incisors,  264 
of  teeth,  macroscopic,  264 
Degenerations,  47 
amyloid,  56 
colloid,  52 
fatty,  48 


I  >egenera1  ions     I  !on1  \l. 
granular,  48 
hyaline,  54 
mucoid,  50 
parenchymatous,  48 
waxy,  bacony,  or  lardaceous,  56 
Dengue,  193 
Dental  band,  241 

Dental    caries    among    civilized    races, 
311 
among  school  boys  and  girls,  313 
and  age,  320 
and  civilization,  311 
and  general  diseases,  321 
and  heredity,  321 
and  inflammation  of  gingiva  and 

gums,  320 
and  meat  diet,  320 
and  pregnancy,  320 
and  starchy  foods,  320 
and  teeth  in  malocclusion,  319 
chemico-bacterial  theory  of,  314 
coarse  foods  in  relation  to,  312 
conditions  which  favor  onset  of,  320 
conditions  which  favor  progress  of, 

317 
constitutional  factor  in,  414 
"dry  mouth"  in  relation  to,  316 
etiologic  factors  in,  322 
factors  which  favor,  314 
historical  data,  306 
immunizing  properties  of  saliva  in, 

315 
immunity    to    in    uncivilized    races, 

311 
in  British  races,  313 
in  candy-makers  and  millers,  312 
in  Maori  race,  313 
in  meat-eating  tribes,  312 
in  prehistoric  times,  311 
on  immunity  from,  315 
pathologic  processes  in,  322 
predisposing  causes  of,  317,  320 
quantity    of   saliva   in   relation    to, 

316 
races  free  from,  312 
restricted,  320 
salivary    stimulants    in    relation    to, 

312 
statistics  on,  313 
Dental  cysts,  532 
ectopia,  304 
disease,  definition  of,  213 

predisposing  causes  of,  215 
follicle,  chronology  of,  245,  254 
follicles  in  syphilitic,  305 
granuloma,  355,  436,  549 
groove,  241 


580 


INDEX 


Dental— Cont'd. 

hypoplasia  and  caries,  252 
hypoplasia,  definition  of,  251 

microscopic,   252 
infantilism,  304 
lamina,    241 
papillae,  246 
ridge,  241 

stigmata  of  syphilis,  303 
Dentrifices,  cause  of  dentin  discolora- 
tion, 347 
Dentigerous  cysts,  410,  441 
Dentin,  228 
caries,  340 

carious  process  in,  326 
caries,   progress   of,   342 
chemical  composition  of,   233 
comparative  hardness  of,  226 
discoloration    by    dentrifices,    347 
elastin  in,  230 
forming  organ,  246 
hypoplasia,  256 
intertubular  substance  of,  248 
lactic  acid  in  depth  of,  328 
matrix,  230 

matrix  liquefaction  of,  342 
microorganisms  in  the  structure  of, 

327 
nature  of  tissue,  228 
nutrition  to,   from  cementum,   237 
pigmentation  in  caries,  347 
secondary,  511 

amorphous,  511 

amorphous  classification  of,  511 

typical,  511 
temporary  arrest  of  calcification  in, 

2.",:: 
the  softening  of,  341 
transverse  section  of,  229 
Dentinal  fibrillar,  228 
tubuli,  228 

a  field  of,  229 

anastomosis  of,  230 

average  diameter  of,  250 

bacteria  in.  238 

calcifications  in,  250 

Calcific  degenerations  of,  510 

curves  of,  231 

in   bicuspids   and  molars,   230 

in  crown  portion,  230 

in  incisal  region,  230 

in  relation  to  cusps,  231 

in  root  portion,  230 

penetration  into  enamel,  232 

penetration  into  cementum,  237 

putrefactive  changes  in,  414 

relative  diameters  of,   230 


Dentinification,  process  of,   247 
Dentition,   complete  absence   of,   202 

deformities  of,  due  to  syphilis,  302 
Dentoalveolar    abscess,    acute    apical, 
424 
acute  osteomyelitis  in,  435 
chronic,  436 

chronic,  bacteria  from,  551 
chronic  forms  of,  438 
chronic,       systemic       involvement 

from,  551 
clinical  symptoms  of,  425 
pathologic  anatomy  of,  433 
Deposit,   calcareous,   381 

subgingival,     lesions     produced    bv, 
392 
Development  of  teeth,  241 
Diagnosis  by  percussion,  440 
Diapedesis,  99 
Diaphanous  halo,  345 
Diathesis,  gouty,  increase  of  chlorides 
in,  372 
hyperacid,  ammonium  carbonate  in, 
372 
Diet  and  caries,  311 
Diphtheria,   173 

Diploeoccus   intracellularis   meningiti- 
dis, 156 
Disaccharides,   32  4 

Discoloration  from  pulp  putrefaction, 
524 
of  enamel,  congenital,  259 
of  teeth,   441 

on    approximal    surfaces    of    bicus- 
pids and  molars,  334 
with  nonexposed  pulp,  530 
Disease,  cause  of,  37 
congenital,  40 
contagious,  152 
definition  of,  21 
dental,  definition  of.  213,  216 
predisposing  causes  of,  215 
etiology  of,  37 
functional,  21,  216 
infectious,  pathology  of,  152 
general,  definition  of,  216 
of   the   gingiva?,   gums    and    mucous 

membrane,  565 
organic,  216 
Diseases  of  peridental  membrane.  402 
nf  suboxidation,  361 
suppurative,  154 
susceptibility  to,  214 
toxemic,  172 
Dropsy,  95 

Ducts  of  salivary  glands,  deposits  in, 
381 


l.M'I.X 


581 


Drugs,  irritating,  in  rool  canal  work, 

408 
1  dysentery,  amebic,  1 B5 
bacillary,   175 

E 

Ear,  involvement  from  impacted  t1iir<l 

molars,    297 
Ecchymosis,  86 

Ectoderm,  35 

tissues  derived  from.  35 
Edema,  84,  95 

angioneurotic,  96 

cachectic,  96 

cardiac,  96 

ex  vacuo,  96 

gaseous,  177 

lymphatic,  96 

malignant.    177 

mechanical,   96 

pulmonary,  96 

renal,  96 

toxic,  96 
Elastin  in  dentin,  230 
Electricity,  effects  of,  43 
Electrolytes,  30 
Elephantiasis,  95,  206 
Emboli,  composition  of,  91 

infectious,  463 

traumatic,  91 

types   of,   90 
Embolism,  90 

results  of,  92 
Embolus,  capillary,   90 

cardiac,    90 

lymphatic,   91 

paradoxical,  91 

venous,  91 
Enamel,  action  upon,  of  dilute  acids, 
219 

agenesia,  256 

and  cementum,  line  of  junction,  22S 

brown  spots  in,  319 

calcification,  effects  of  exanthemata 
upon,  253 

calcification  installments,   221 

caries,  etiology  of,  331 
first  symptom  of,  332 
localization  of,  334 
photomicrograph  of,  333 

cementing  substance   in,   219 

chalky.  258 

character    of    external    surface    of, 
225 

chemical  composition  of,  223 

comparative  hardness  of,  226 

complete  or  partial  absence  of,  255 

components  of,  219 


Enamel  — <  font  'd. 
deciduous,  when  it  begins  to  form, 

246 
defects    in,    from    insufficiency    of 

structure,   319 
deviations  in  quantity   and  quality 

of    interprismatic    Bubstanee, 

253 
direction   of  calcification   of,  246 
dissolution  of,  in  carii  s.  .".22 
fissures  in,  225 
granular  defect  of,  263 
hypoplasia    of,    producing    external 

defect,    255 

hypoplastic,  and  earies,  317 
in  abnormal   locations,  286 
imbrication  lines  of,  224 
imperfect,     where     frequently     en- 
countered, 258 
interprismatic     substance     of,     sus- 

eeptibility  to  acids,  219 
malacotic,  mass  density  of,  226 
native,  mass  density  of,  226 
normal,   description  of,   217 

microscopic   appearance   of,   217 
pearl,  286 

of  primitive  races,  225 
organ,  functions  of  layers  of.  246 
layers  of,  244 

of  second  permanent  molar,  245 
time  of  appearance,  for  decidu- 
ous teeth,  2  15 
origin  of  word,  223 
porosity  of,  226 

perfection  in  development  of,  217 
permeability,  degrees  of,  226 
pit  form  defect  of,  263 
reddish  brown  discoloration  of,  259 
ridges  and  furrows  in,  223 
rods,  description  of,  219 

imperfect    calcification   of,   253 
insufficient   formation   of,  260 
on  axial  surfaces,  220 
under  high  magnification,  220 
washing  away  of,  332 
sclerotic,  mass  density  of,  226 
surface,  not  smooth,  223 
temporary  arrest  of  calcification  in, 

253 
thickness,  variations   in,   218 
unvarying  hardness  of,  228 
white  spot  in,  258 
Enameloblasts,  245 

Endocarditis  from  oral  foci  of  infec- 
tion, '<''■'■ 
Endothelia,  36 
Endotheliomata,   146 
Endotoxins,  153 


582 


INDEX 


Entameba  histolytica,  185 
Enterorrhagia,  85 
Entoderm,  35 

tissues  derived  from,  36 
Eosinophils,  99 
Epistaxis,  85 
Epithelial  band,  24 

cells  in  pulp  hypertrophy,   531 

cord,  241 

invagination  of,  244 

debris,  407 

remnants   in   peridental   membrane, 
527 
Epithelioma,  141 
Epithelium   of  gingiva?,   functions   of, 

379 
Equinia,  171 

Erosion    bv    sodium    acid    phosphate, 
360 

duplication  in  laboratory,  359 

etiology  of,  359 

from  lactic  acid,  360 

pathologic  anatomy  of,  365 
Erysipelas,  156 
Erythrodextrin,  322 
Etiology,  definition  of,  213 

of  abrasion,  356 

of  caries,  322 

of  diseases,  37 

of  emboli,  93 

of  enamel  caries,  331 

of  erosion,  359 

of  geminated  teeth,  284 

of  septic  apical  pericementitis,  415 
Eustrongyles  gigas,  206 
Extractions,   tooth   movement    follow- 
ing, 379 
Exudate,  inflammatory,  99 

inflammatory  serous,  435 
Exudation,  95 

Eye  involvement  from  impacted  third 
molars,   297 

F 

Face,  involvement  of,  in  dentoalveolar 

abscess,  429 
Facial     pain     from     impacted     third 

molars,  297 
False  membranes,  74 
Fatty  degeneration,  48 
Fatty  infiltration,  59 
Favus,  183 
Fermentation,  lactic  acid  from,  315 

of  carbohydrates,  degrees  of,  323 

of  glucose,  323 

of  lactose,  323 


Fertilization,  34 
Fetor  of  breath,  389 
Fever,  sestive-autumnal,  189 
quartan,  189 
relapsing,  179 
Rocky  Mountain,  195 
tertian,  189 
Texas  cattle,  189 
typhus,  194 
yellow,   193 
Fibers,  encased  in  cementum,  234 
Fibrilla?,  dentinal,  228 
Fibrin  ferment,  74 
Fibroadenoma,  139 
Fibroblasts,  99,  108,  406 

of  repair,  443 
Fibroids,  recurrent,  127 
Fibroma,  uterine,  131 
Fibromata,   117 

soft,  118 
Filariasis,  205 
Fissures,  caries  in,  334 

defective,  calcified  amorphous  bodies 

in,  200 
defective,  in  molars  and  bicuspids, 

318 
perfect,  in  molars  and  bicuspids,  318 
Flatworms,  195 
Focal  necrosis,  78 
Foci  of  infection,  544 
chronic,  422 
endocarditis  from,  553 
extraosseous,   549 
intraosseous,    549 
most    common,    551 
oral,  arthritis  from,  553 
secondary,  562 
Follicular  cysts,  534 

pathologic,   anatomy  of,    540 
sac,  247 
wall,  233 

functions  of,  248 
Foot  and   mouth  disease,  194 
Formaldehyde,    irritation    by,    408 
Fractures,  intraalveolar,  of  roots,  419 
Frostbite,  42 
Functions  of  gingiva?,  378 

of   peridental   membrane,   402 
Fungus  hematodes,  145 
Furuncle,  103 


G 


Gallstones,   70 
Gangrene,  79 
dry,  79 
moist,    79 
of  pulp,  523 
primary,  79 


I  MUX 


583 


i  Sangrene-    <  fonl  'd. 

36C Inry,     7!' 

senile,  s" 

ma  edema,  177 
Gelatinous  plaques,  331 
Germicidal   concentrations,  effects  of, 

409 
Germicides,   mild,    in    root    infections, 

410 
Geminated,  deciduous  teeth,  284 
Geminated  teeth,  284 
Germ  plasm,  40 
Giant  cells,  of  repair,  107 
Gingiva,  relation  to  peridental  mem- 
brane, 403 
Gingiva?,  body  of,  376 

chronic    inflammation    of,    photomi- 
crograph  of,   395 
classification  of,  376 
free,  377 

functions    of,    378 
internal   aspect   of,    379 
normal    and    pathologic    considera- 
tions, 376 
peridental  membrane  fibers' in,  377 
septal,   377 
of  sheep,   376 
Gingival  epithelium,  functions  of,  379 

irritation,   391 
Gingivitis  by  salivary  deposits,  389 
chronic,  392 

advanced,       p  h  o  t  o  m  i  c  rograph 

stage,   396 
progressive    photomicrograph    of, 

398 
pathologic  anatomy  of,  392 
involvement     of     peridental     mem- 
Inane  fibers  in,  393 
Glanders,  171 
Gleet,  157 
Glioma,  132 

ganglionic,  133 
Globulins,  28 

Glucose,   fermentation   of,   323 
Glycogenic   infiltration,   71 
Glycoproteins,    28 

Glycosuria,   artificially   induced,   man- 
ifestations in   saliva,   374 
Gonorrhea,   157 
Goutv  diathesis,  increase  of  chlorides 

in,  372 
Granular   degeneration,  48 
Granular   layer   of   Tomes,    231 

relation  of  to   dental  caries,   .r;2H 
Granulation  tissue   in   pulp   hypertro- 
phy, 530 
Granuloma,"  dental.  423,  355,  436.  549 
objections  to  term,  438 


Granulomata,    infectious,    164,   438 

Growth,  giant,  111 

Guinea  worm  disease,  205 

Gum    recession,    attempts   to   reme.lv, 

388 
Gumma,  170 
( in  ins  and  gingiva?,  '■'>''< 

blood  supply  of,  375 

histology  of,  375 

II 

Habits,  as  a  predisposing  cause,  40 

Haplobaeteria,   153 

Hard  and  soft  teeth,  226 

Harelip,  211 

Healing  by  first  intention,  106 

by  second  intention,  106 

by  third  intention,  107 
Health,  definition  of,  21 
Heat,  exciting  cause  of  disease,  41 

exhaustion,  42 
Helminthes,  195 
Helminthiasis,  195 

Hematogenic    route,    periapical    infec- 
tion by,  421 
Hemangiomata,  134 
Hematidrosis,  85 
Hematocele,  85 

Hematogenous  pigmentation,  63 
Hematoidin,  66 
Hematoma,   86 
Hematemesis,  85 
Hematuria,  85 
Hemoglobin,  29,  66 
Hemopericardium,   85 
Hemoperitoneum,  85 
Hemophilia,  87 
Hemoptysis,  85 
Hemorrhage,  85 
Hemorrhagic  infarct,  86 
Hemorrhage,   secondary,   86 
Hemosiderin,   64,   66 
Hemothorax,   85 
Hepatization,  160 
Hepatogenous   pigmentation,   63 
Heredity  and  absence  of  teeth,  291 

and  caries,  321 

and  disease,  40 
Herpes  labialis,  572 
Heterolysis,  76 
Heteroplasia,  110 
Histologic  defects  in   enamel,   253 
Histology,  morbid,   definition   of,   213 

of  gums  and  gingivae,  375 

pathologic,  37 
Howship  's  lacuna?,  470 


584 


INDEX 


Hutchinson's  notch,  266 
teeth,  269,  299 

triad,  304 
Hyaline  degeneration.  54 
Hyaloplasm,  25 
Hydrocephalus,  96 
Hydropericardium,  96 
Hydroperitoneum,  9(5 
Hydropic  infiltration,  71 
Hydrops,  articuli,  96 
Hydrorrhaehis,  96 
Hydrothorax,  96 
Eylomata,  116 

Hyperacid   diathesis,    ammonium   car- 
bonate in,  372 
Hypercementosis,  350 

and  pulp  removal,  355 

and  pyorrhea  alveolaris,  355 

causes  of,  353 

etiologv    and    pathologic    anatomy, 
352 

from  mild  infection,  354 

from  occlusion  stress,  353 

from    protruding   root   filling,    354 

from  rough   edges   of  fillings,   353 

from   salivary   and   subgingival   de- 
posits, 353 

from  thread  biting,   353 

from  tooth  movement,  353 

in    chronic     dentoalveolar     abscess, 
354 

in  lower  molars,  351 

in  upper  bicuspids,   351 

in  upper  molars,  351 
Hyperemia,  83 

active,  83 

collateral,  83 

neuroparalytic,  83 

neurotic,  83 

of  pulp,  505,  518 

passive,   84 
Hypernephroma,   14^ 
Hyperostoses,   121 
Hyperplasia,   111 
Hypertrophy,  111 

'false,   111 

numerical,  111 

of  pulp,  530 

simple,    111 

true.  111 
Hyphomycetes,   152 
Hypoplasia,  45,  250 

of  cervieo-lingual   ridge,   205 

dental,  causes  of,  252 
microscopic,   251 
milder  forms  of,  260 
pathologic  anatomy  of.  258 
of  deciduous  teeth,  258 


Hypoplasia — Cont'd. 

of  dentin.  256 

of  enamel  and  caries,  317 

of    enamel   producing    external    de- 
fect, 255 

of  lower  first  bicuspid,  277 

of  lower  cuspid,  270 

of  lower  second  bicuspid,  277 

of  upper  cuspid,  269 

of  upper  third  molar,  283 
Hypoplastic  enamel,  predisposition  to 
causes  of,  318 


Idiosyncrasy,  39 

Imbrication   lines   and   caries   suscep- 
tibility, 225 
Immune,  saliva  of,  315 
Immunity,   153 
acquired,  153 

from  dental  caries  on,  315 
natural,    154 
Impaction   of   third   molars,   case   his- 
tories, 296 
Incisor  central,  abrasion  of,  362 

disproportion    in    size    of    crown 

and   root,   266 
imperfect    development    of    root, 

266 
macroscopic  deformities  of,  264 
overdeveloped,    266 
supernumerary  root  in,  265 
with  short  root,  267 
lower  lateral,  abnormalities  of,  269 
lower    central,    freedom    of    defects 

of,  267 
upper  lateral,  abnormalities  of,  267 
absence  of,  291 
deflection  of  root  of,  268 
peg-shaped,   268 
Incisors,  abrasion  in,  358 

supernumerary   tuberculated,   287 
Incremental   lines,   221 
Endol,  524 

Infantile  paralysis,  192 
Infantilism,   45 
Infarcts,  92 

anemic  or  white,  92 
hemorrhagic,    86 
hemorrhagic  or  red,  93 
Infection,   152 
Infectious  protozoa,  185 
Infestation,    152 

Inhibition,   pain   a   source  of,   294 
Infiltration,   59 
calcareous,   68 
fatty,  59 


I\IU  \ 


585 


I  nlilt  rat  inn      ( 'nut  'd. 

glycogenic,   71 

hydropic,   70 

intiTst  it  Lai,  of  fluid,  95 

pigmentary,  61 

round  eell,  99 

serous,   70 
Inflammation,  08 

acute,  98 

acute,  characteristics  of,  99 

catarrhal,  104 

chronic,  98 

ehronieity  and   acuteness  of,  424 

diphtheritic,  100 

edematous  or  serous,  100 

fibrinous,  100 

follicular,   105 

hemorrhagic,  106 

interstitial,    106 

of   gingiva    and    gums    and    dental 
caries,  320 

parenchymatous,   105 

phlegmonous,   103 

phlegmonous,  of  face,  431 

productive,   106 

septic,  of  peridental  membrane,  412 

suppurative,  101 
Inflammatory  exudate,  09,  435 
Influenza,  178 
Interglobular  spaces,   231 

abnormal  in  size  and  number,  256 
abundance  of,  319 
Interprismatic    substance,    dissolution 
of,  325 
susceptibility  to  acids,   219 
Interproximal  spaces,  flat,  319 
Ionization,  30 
Irritability,  32 
Irritation  by  formaldehyde,  408 

gingival,  391 
Ischemia,  82 


Jaws,    necrosis,    bacterial    causes    of, 
464 
chemical   causes  of,  464 
diagnosis  of,  463 
mechanical  causes  of,  463 
osteitis  of,  470 
osteomyelitis  of,  469 
periostitis  of,  467 
rarefying  osteitis  of,  462 


K 


Karyoplasm,  25 

K-iryosomes,  26 
Keloids,    117 


Lactic  acid,  end  producl  of  fermenta- 
tion, 315 

in  depth  of  dentin,  328 

in   erosin,  360 
Lactose,    fermentation   of,   323 
Lacuna:  of  cementum,  233,  235 
Lamellae  of  cementum,  233 
Leishmaniases,    187 
Lepedomata,    1  Hi 
Leptothrix   infections,   180 
Leprosy,  167 
Leptus  autumnalis,  206 
Leucin,  524 

Leucocytes    in    chronic    dentoalveolar 
abscess,  444 
mononuclear,    448 
polymorphonuclear,   99 

eosinophil,   447 

neutrophile,  444 
Leucoplakia  of  tongue,  573 
Leukoderma,   67 
Life,  simpler  forms  of,  26 
Lime  salts,  extraction  of,  from  teeth 

316 
Linin,    26 
Lipoids,  29 
Lipomata,   122 
Liquefaction  necrosis,  75 
Lock  jaw,   172 
Lues,  168 
Lumpy  jaw,    181 
Lung  dust  disease,  61 
Lymphangiomata,    135 
Lymphatic   vessels,  obstruction  of,  95 
Lymphocytes,  99,  447 
Lymphosarcoma,  125 
Lysins,   153,  76 

M 

Macroscopic    pathology,    37 

Madura  foot,  182 

Malacotic    enamel,    mass    density    of, 

226 
.Malaria,  187 

Plasmodium  of,  187 
Malarial   pigmentation,   62,   63 
Malformations,  208 

by  defect,   208,  209 

by  excess,  208 

by  perversion,  208,  211 

due    to    defective    development    in 
anterior    median   line,    209 

due     to    defective    development    in 
posterior  median  line,  209 
Malignant   edema,   177 
Malocclusion    ami    abrasion,   356 

and    dental    caries,    319 


586 


INDEX 


Maltose  from  starch,  322 

Maori  race,  caries  in,  313 

Malta  fever,  176 

Maltase  enzyme,     - 

Maltose,  hydrolysis  of,   32 

Mummification,  79 

Mandible,    sinuses   on    lingual   aspect, 

429 
Marrow.  456 
red,  456 
yellow,  456 
Matrix  of  eementum,  2:;4 
Maxillary    sinus,    abscess    discharging 
'into.   427 
infection  from  cell.   427 
variations  in  shape  and  size.  427 
Measles,  190 
black,  190 
German,  191 
Meat  diet  and  dental  caries,  320 
Meat-eating  tribes  and  earies,  -'112 
Medullary  substance,  458 
Melanocarcinoma,  146 
Membranes,  false,  74 
Meningitis,     epidemic     cerebrospinal. 

156 
Menorrhagia,    85 
Mercurial  stomatitis,  569 
Mesoderm,   35 

tissues  derived  from,  36 
Metabolic  pigmentation,  62 
Metaplasia,  110 
Metaplasm,  25 
Metastasis.  92 
Metazoa.  152.  195 

i  hagia,  s5 
Micrococcus  gonorrheal,  157 

tetragenus,   1~>~> 
Microorganisms,   pathogenic   for  man. 

152 
Microscopic   pathology,   37 
Mites,  196 

Molars    and    bicuspids,     discoloration 
on   approximal   surfaces,   334 
defective  fissures  in,  318 
first  permanent,  disturbances  affect- 
ing development  of,  253 
noneruption  of,  293 
fourth,  289,  290 

impacted  third,  and  disturbed  pho- 
nation,  298 
ear  involvement  from,  297 
eye  involvement  from.  2T»7 
facial  pain  from.   297 
lower    first,    disto  buccal    cusp,    ab- 
sence of,  281 


Molar 

lower  first,   supernumerarv  root  in, 

281 
lower,  hypereementosis  in,  351 
lower  second,  abnormalities  of,  282 
lower  second,  with  four  roots,  282 
lower  third,  dwarfed,   282 
lower  third,  supernumerarv  root  of, 

283 
second,  impaction  of,  297 
second  permanent,  origin  of  enamel 

organ  of,  245 
third   permanent,   origin   of   enamel 

organ  of.   245 
perfect  fissures  in,  318 
supernumerary,    289 
third,  upper  and  lower,  abnormali- 
ties of,  283 
impacted.   294 

case  histories,   296 
reflexes   from,   294 

reflex  disturbances  from.  296 
upper  first,  fusion  of  roots  of.  230 
supernumerary  cusp  in,  280 
hypereementosis  in.  351 
second,   abnormalities   of.   281 
third,  dwarfed.  2^2 
hypoplasia  of,  283 
supernumerarv  root  in,  284 
Molds,  152 
Mole  pigmented.  135 
Molluscum  contagiosum,  142 
Mononuclear    wandering    cells,    origiu 

of.  449 
Monosaccharides.  324 
Morbid  anatomv. 
Morula,  34 
Motility,   32 

Mouth  bacteria,  number  of,  315 
infection  and  cancer.  561 
and   systemic   disease,   544 
and   tuberculosis.   561 
as  a  source  of  systemic  intoxica- 
tions,   '>'>') 
dry.  and  dental  caries,   316 
washes,  weak  acids  in,  332 
Mucin,  28,  369 

in  plaque  formation.  331 
precipitation  of,  370 
Mucoid  degeneration. 
Mucous    membrane    of    gingivae    and 
gums,   375 
of  hard  palate.  375 
patch,  136 
Mumps,  191 
Mycetoma,   182 
Mycoses,  152,  180 
Myxomata,   119 


IN  D IX 


:»7 


N 

NaCI,  increased,  95 

Nanism,    15 

Xasal  cavity,  abscess  discharging  into, 

127 
Nasmytb  *s  membrane,  246 
Necrobiosis,  72 
Necrosis,  72 

coagulation,  7:; 

Eat,  77 

focal,  78 

liquefaction,   II,  75 

cheesy,  76 

of  alveoli,   462 

of  jaws,  bacteria]  causes  of,  464 
causes  of,  463 
chemical   causes  of,  464 
diagnosis  of,  463 
mechanical  causes  of,  463 
Nematodes,  196 
Neoplasm  of  pulp,  508 
Nevus,  135 
Neuridin,  413,  524 
Neurin,  413 

Newman,  sheaths  of,  230 
Nitrogenous  decomposition,  413 
Nodules,  pulp,  514 
Nonelectrolytes,  30 
Nucleolus,  26 
Nucleoplasm,  26 
Nucleus,  2-1 


0 


Occlusion       stress,       hypercementosis 

from,   353 
Occupations,   injurious,   40 
Odontoblastic  layer,  230 
Odontoblasts,  247,  500 
Odontomas,  cystic,  532 
Oidiomycosis,  183 
Opsonins,   153 

Ophthalmia  neonatorum,  157 
Oral  disease,  definition  of,  213 
Oral  foci  of  infection,   544 
Organic  disease,  216 

matter,     comparison     in     cementum 

and  bone,  240 
Osmosis,  disturbed,  95 
Osteitis,   of  jaws,  470 

rarefying,  462 
Osteoblasts,  407 
Osteoclasts,  4n7,  456 
Osteogenetic  laver  of  periosteum,  456 
Osteomalacia  of  pregnancy,  causes  of, 

320 


Osteomata,  121 

heteroplastic,  121 

homoplastic,  121 
Osteomyelitis,  394 

acute,  in  dentoalveolar  abscess,  i:;r,, 
157,  469 
Osteophytes,  121,  467 
Oxuris  vermicularis,  202 
Oxygen    ten-inn,    change    of,    in    root 
canal,  414 


Pain,  continued,   action  of,   204 
Palate,    hard,    mucous    membrane    of, 

375 
Papilla,  dental,  246 
Papillomata,   135 

hard,   136 

intracystic,  136 

soft,   136 
Paralysis,  infantile,  192 
Paraplasm,  25 
Parasites,   152 

facultative,    152 
Parenchymatous    degeneration,    IS 
Parotitis,  acute  epidemic,  191 
Parules,  431 
Pasommoma,   147 
Pathologic  anatomy,  37 
definition    of,  *213 
of    chronic   gingivitis,    392 

chemistry,  37 
Pathology,   cellular,   123 

dental,  definition,  213 

general,  definition,   21 

general   and    dental    conception   of, 
216 

gross,  37,  216 
Pathologic  histology,  37 

physiology,  216 

processes,  45 
Pediculus  capitis,  196 

pubis,  196 

vestimenti,  196 
Petechia?,  86 
Peptides,  27 
Peptones,  27 

Perforations  of  root  canals,  419 
Periapical    infection    by    hematogenic 

route,  421 
Periapical   infections,   recovery   from, 

422 
Pericemental  abscess,  422 
of  gouty  origin,  496 

inflammation,   acute  septic,  412 
septic,  412 
septic,   summary   of  causes,   421 


588 


INDEX 


Pericementitis,  acute  septic,  412 
chronic   septic,  412 
first  symptoms  of,  433 

nonseptic,    Mis 

aonseptie,  caused  by  protruded  root 

fillings,  410 ' 
nonseptic,  causes  of,  408 
nonseptic,    from    arsenic,    4ln 
nonseptic  from    pressure,   410 
nonseptic,    from    pulp    extirpation, 

410 
septic  apical,  422 
bacteria  of,  452 
etiology  of,  45 
Pericementum,  402 
Peridental  membrane,   IMS 
apical   fibers,   406 
atrophy  of,  491 
blood  "supply  of,   402,  407 
cysts   from   chronic    infection   of, 

441 
diseases  of,  402 

effect  of  mild  irritation  upon,  352 
epithelial  remnants  in,  442,  527 
fibers  of,  404 

fibers,  detachment  of,  439 
free  gingiva  fibers,  406 
functions  of,  402 
horizontal  fibers  of.  405 
involvement  in  gingivitis,  393 
nerve  supply  of,  407 
oblique  fibers  of,  405 
relation  of,  to  gingiva,  403 
septic   inflammation  of,  412 
structural  constituents  of,  406 
susceptibility   to   infectious   proc- 
esses, 402 
transseptal  fibers,  406 
thrombi  in,  410 
Periosteum,  456 

Periostitis,  acute,  in  dentoalveolar  ab- 
scess,  431,   435 
Pernio,  42 
Pertussis,   179 

Periostitis,     chronic,     osteophytes    in, 
467 
of  jaws,  acute,  467 
symptoms  of,  469 
syphilitic,  470 
Phleboliths,  381 
Phonation,    disturbed,    from   impacted 

third  molar,  298 
Phosphoproteins,  29 
Physiochemical    processes    in    tissues, 

21 
Physiology,    pathologic,    definition    of, 

213 
Pickerills'  calearine  fissures,  225 


Pigment,  malarial,  63 
Pigmentary  infiltration,  61 
Pigmentation,  hematogenous,  63 

hepatogenous,  63 

malarial,   62 

metabolic,  62 

of  dentin  in   caries,   '117 
Pigments,   metabolic,    63 
Pits,  caries  in,  334 
Plague,  bubonic,  177 
Plaque    formation,    mucin    in,    331 
Plaques,  gelatinous,  331 
Plasma  cells,  99,  451 
Plasmodium   malaria1,    187 
Plastids,  25 
Platyhelminthes,  195 
Pneumonia,  159 

aspiration,    163 

fibroid,  163 

hypostatic,   163 

lobar  or  croupous,  159 

lobular,   161 

purulent,  163 

tuberculous,  164 
Pneumonokoniosis,  61 
Pocket  formation,  bone  lesion  in,  39  I 
Poisons,  chemical,  44 
Poliomyelitis,    acute,    192 
Polyarthritis.  193 
Polymorphonuclear  leucocytes,  445 
Polysaccharides,  325 
Poulticing,   results  of,  428 
Predisposing   causes,   213 
of  dental  caries,  320 
Pregnancy  and  dental  caries,  320 
Pressure,  effect  of,  41 
Processes,  retrograde,   45 
Protamines,  28 
Proteins,  27 

conjugated,  28 

simple,  28 
Proteoses,  27 
Prothrombin,  74 
Protoplasm,  23 
Protoplasmic  movement,  32 
Protozoa,  23,   152 

classification  of,   185 
Pseudomelanin,  63 
Pseudomucin,  52 
Ptyalin,  370 

role  in  caries,  370 
Pulex  eheopis,  196 

irritans,  196 

lipines,   196 

penetrans,  196 


i.\i)i;.\ 


589 


Pulp  abscess,  530 
areas   of   chronic    inflammation   in, 

507 
blood  vessels  of,  504 
calcific  degenerations  of,  510 
cells  of,  503 
description  of,  500 
clinical  aspect  of  diseases  of,  505 
congestion,  521 
constructive  changes  in,  506 
death,  chemical  causes  of,  523 
death,  mechanical  causes  of,  523 
death  of,  en  masse,  523 
decomposed,  413 
degenerations,  508 
degeneration  in  abrasion,  358 
diseases  of,   505,   500 

exciting   causes,   general,   508 

exciting  causes  of  (local),  509 

local   predisposing  causes  of,  507 

predisposing  causes  of,  506 
exposure   in   abrasion,    357 
gangrene,  523 

gangrenous,  organisms  in,  452 
histologic  constituents  of,  500 
hyperemia,  505,  518 

active,  518 

character  of  pain  from,  522 

etiology  of,   520 

following    insertion    of    gold    fill; 
ings,  521 

from  erosion  and  abrasion,  521 

in  febrile  disturbances,  508 

passive,  518 
hypertrophy,     calcareous     formations 
in,  530 

epithelial  cells  in,  531 
impairment   of   vitality,   505 
infection  in  absence  of  caries,  527 

ulcerative   form,   530 
intercellular    substance    of,    504 
involvements,  prophylaxis  of,  414 
lead-wire  formation  in,  517 
live,   abscess  in  teeth  with,  422 
moist  gangrene,  524 
mummification,   523 
neoplasm,  508 
nerves  of,  504 
nodules,   514 

from  erosion  and  abrasion,  517 
normal,  501 
Pulp,  odontoblastic  layer  of,  230 
putrefaction,   413 

discoloration  from,  524 

products  of,  524 
putrefactive  changes  in,   525 
putrescent,  523 

organisms  in,  524 


Pulp     Cont'd. 
removal  and  hypercementosis,  355 

reparative  power  of,  .~ u i t 
retrograde  changes  in,  506 
severe   inflammation   of,    ) l'.~ 
suppurating,  organisms  in,   152 
suppuration,   1 13,  528 
temperature,  range  of,  520 
thrombosis  in,  523 
Pulpitis,    525 

chronic    hypertrophic,    530 
nonseptie,   525 

pathologic    anatomy    of,    528 
septic,  526 

character  of   pain    in,   527 
Pus,  101 
Pus   pocket,   394 
Pustule,  103 
Putrefaction   of  pulp,   413 

products  of.  524 
Putrefactive   changes   in    dentinal    tu- 
buli,  414 
changes  in,  pulps,  525 
Putrescin,   413,   524 
Pyemia,   103,   154 
Pyogenic    bacteria    in    apical    region, 

412 
Pyorrhea  alveolaris   and   hypereemen- 
tosis,    .'!•"." 
and    malposition   of   teeth,   379 
bacteria  in,  551 
bacteriology  of,  491 
by  salivary  calculi,   474 
by   subgingival   deposits,   476 
clinical    forms,    473 
defective  approximal  contacts  in, 

479 
food  impactions  in,  476 
general  considerations,  473 
historical  sketch.  471 
indicative  of,  473 
of  gouty  origin,  495 
of   systemic    origin,   487 
osteomyelitis  in,  484 
substitute  terms  for,  473 
systemic  disorders  and.  485 
systemic  factor  in,  490 
systemic      lesions      by      bacteria 
from,  551 
pockets,  study  of  culture  of,  494 

E 

Race  as  a  predisposing  cause,  39 
Rarefaction  areas,  419,  554 
Rarefying  osteitis,  462 

of  alveoli,  462 

of  jaws,  462 


590 


INDEX 


Raynaud's  disease,  82 

Eeflexes  from  impacted  third  molars, 

294 
Regeneration,   108 
pathologic,  108 
physiologic,   108 
Renal  calculi,  70 
Relapsing  fever,  179 
Re]  roduction,  33 
Resorption  of  apical   areas,   465 

of  eementum,   250 
Retrograde   processes,   45 
Retzius,  bands  of,  221 
in   hypoplasia,  262 
Ridge,  cervieolingual  fissured,  265 
Rhabdomyoma,  1 30 
Rheumatism,    acute    articular,    192 
Rhinoscleroma,   171 
Rhinoliths,    70 
Rigos'  disease,  473 
Ringworm,  183 
Rocky  Mountain  fever,  195 
Rodent  ulcer,  142 
abrasion  of,  357 

bifurcation  in   uppar  second   bicus- 
pid, 27:; 
cysts,  532 

deflection    in    upper    first    bicuspid, 
271 
Root 

canals,   irritating   drugs   in,   408 

perforation   of,   419 
of    central    incisor,     imperfect     de- 
velopment of,  266 
filling    beyond    apical    foramen,    ef- 
fects of,   353 
fractures,    intraalveolar,    419 
fusion  of,  in  upper  first  molar,  280 
of    upper    second    bicuspid,    abnor- 
malities  of,   271 
perforation,  411 

supernumerarv,    in    central    incisor, 
265 
in    lower    cuspid,    273 
in  lower  first   molar,  281 
in   lower  third  molar,  283 
in  upper  third  molar,  284 
two,  in  lower  bicuspids,  277 
in    lower    cuspid,    270 
in  lower  cuspids,   272 
in  lower  lateral  incisor,  269 
in  upper  second  bicuspid,  274 
Rubeola,' 190 

S 

Saccharomyces  albicans,  571 
Saliva,    366 

abnormal  constituents  of,  373 


Saliva— Cont'd. 

action  on  blood  cells,  315 

albumin  in,  371 

amount  of,  366 

color  of,  in  pathologic  and  normal 

states,  367 
hemolytic  power  of,  315 
immunizing  properties  of,  315 
immunizing  properties  of,  and  den- 
tal  caries,    315 
inorganic  constituents  of,   369,  372 
manifestation  in,   of  excessive  car- 
bohydrate intake,  374 
odor   of,  in  pathologic  and  normal 

states,  368 
of  immunes,  315 
of  immunes  to  caries,  '■'<  1 5 
of  susceptibles  to   caries,  316 
on   antiseptic  power   of,   315 
organic   constituents   of,   369 
parotid,    unmixed,    383 
quantity    of,    in    relation    to    caries, 

316 
reaction  of,  373 
solution  of  blood  cells  by,  315 
sulphocyanates  in,  371,  372 
taste  of,  in  normal  and  pathologic 

states,  368 
viscosity  of,  316 

in   relation  to  caries,  316 
Salivary  calculus,  agglutinin  of,  384 
destruction    of    investing    tissues 
by,  388 
Salivary 

deposits  and  hypereementosis,  353 
as  cause  of  gingivitis,  389 
clinical  symptoms  of,  389 
color  of,  386 
denudation  of  eementum  by,  388 

effects    Of,    389 

from  betel-nut   chewing,   383 

in   salivary    glands,    381 

lesions   caused    by.   :;s7 

location   of,   381 

origin  of,  381 

size  of,  386 

theories  on  formation   of,  381 

where    first    formed,   388 
depressants,    366 
depressants     of     potential     acidity, 

312 
glands,  deposits  in,  381 
stimulants,  366 

in  relation  to  caries,  :!12 
Sapremia,    151 
Saprophytes,  152 


INDEX 


591 


Saprophj  t  ic  bactei  ia,  action  of,    1 1  '■'■ 

organisms    in    acute    dentoalveolar 
abscess,    133 
Sarcoma,  alveolar,  125 

gianl  celled,   128 

melanotic,  127 

round   cell,    124 

spindle-celled,  127 
Sarcomatous    cylindromata,    126 
Scarlatina,   H'l 
S.-arlct   fever,    191 
Scalorrhea,  367 
Schizomycetes,    152 

Scler eter,  enamel,   228 

Sclerotic  enamel,  mass  density  of,  226 

Secondary   denl in.  ."1 1 

"  Self -cleaning, "  as  applied  to  teeth, 

319 
Septal  gingivae,  377 
Septal  tissues  and  caries,  337 
Septic      pericemental       inflammation, 

acute,  112 
Septicemia,  154 
Sequestrum      formation      in      chronic 

dentoalveolar  abscess,  4(38 
Serous  infiltration,   71 
Serum,  antidiphtheritic,  173 

antitetanic,  172 
Sharpey's  fillers,    156 
Sheaths  of   Newman,  230 
Shock,  41 

Shreger,  lines  of,  222 
Sialorrhea,  .".'';7 
silicosis,    64 
Sinus   formation,  427 
Sleeping   sickni  ss,   186 
Smallpox,   194 
Sodium    phosphate,    acid,    in    erosion, 

360 
Solution,  30 
Somatic  death,  73 
Specific  gravity  of  enamel,   compared 

■with    density,    22<i 
Sphacelous,  7:: 

Spirillum  cholera  Asiatic®,  17". 
Spirocheta  pallida,  168,  305 
Spirochetae  obermeieri,  179 
Spongioplasm,  2."i 
Sporotrichosis,  184 
Sporothrix,  184 
Stain,  brown,  of  enamel,  2-"i9 
Staphyl  coccus  epidermidis  albus,  1~>."> 

pyogenes   albus,    155 

pyogenes    aureus,    155 
Starch,  325 

conversion   of,  into  maltose,  322 
Starchy  foods  and  dental  caries,  320 
Stellate   reticulum,   244 


Stomatitis  aphthous,  570 

pathologic   anatomy  of,  570 

catarrhal,  566 

pathologic   anatomy   of,   567 

mercurial,    "><i'.» 

simple,  565 

pathologic  anatomy  of,  566 

simplex,  565 

ulcerative,  567 

pathologic    anatomy,    ~>t'u 
Stratum   intermedium,  2  I  I 
Streptococci,   in   chronic   dentoalveolar 

abscess,  452 
Streptococcus  erysipelatis,   156 
mucosus,  4o2 
pyogenes,   155 
rheumaticus,   156 
viridans,    156,  452,   551,  552 
Stricture,  157 

Strongyloides   intestinalis,    202 
Subgingival  deposits,  390 

and    hypereementosis,    353 
color  of,  390 
detection   of,  ::!»2 
etiology  of,  390 
lesions  produced  by,  '■'<'.>- 
preliminary     step     in     formation, 
396 
-pa.,,     bacterial    absorption    from, 
380 
penetration   of   bacteria   through, 
422 
Submental    fistula.    430,   4:;4 
Sugars,  double,  324 

multiple,  325 
Sugars,  relative  fermentability  of,  323 

simple,  324 
Sulphocyanates,  amount  of,  in  saliva, 

'  372 
"Sulphur  granules,"   181 
Sunburn,  43 

Sunlight,  bactericidal  action  of,  43 
Sunstroke,   42 

Supernumerary    cusp     in     upper    first 
molar,   280 
molar,  289,  290 
peg-shaped  tooth,  287 
root  in  central  incisor,  26."> 
root  in  lower   first   molar,   281 
root  in   upper  third  molar,   284 
tuberculated  incisors,  287 
teeth,  287 
Suppurative   inflammation,   101 
Suppuration,  description  of,  413 

in   pulp,  413 
Swelling    from    dentoalveolar    abscess, 
431 


592 


INDEX 


Syphilis,    168 

dental  manifestations  of,  transmis- 
sion to  fetus,  253 

hereditary,  dental  stigmata  of,  303 

pathognomonic    signs   of,  303 

primary  stage,   169 

secondary  stage,  160 

tertiary  stage,  169 

transmission  of,  299 
Syphilitic    stigmata,    299 
Syringomyelia,  96 

T 

Tapeworms,    195,    WS 
Teeth,  abnormalities  of,   250 

abraded,  discoloration  of  dentin  in. 

347 
absence    of,    291 
calcium   salt   content   of,   226 
classification  of,  as  to  hardness,  226 
deciduous,    calcification    of,    248 
geminated,   284 
hyperplasia  of,  258 
retention  of,  291 
time  of  appearance  of  enamel  or- 
gans for,   24." 
development  of,  241 
extraction  of  lime  salts  from,  316 
fully  calcified,   noneruption  of,   294 
geminated,  284 
Hutchinson 's,    299 
macroscopic   deformities  of,   264 
malposition  in    pyorrhea  alveolaris, 

379 
mass  density  of.  227 
permanent,   calcification   of,   248 
"  self  -cleansing, ' '  319 
specific  gravity  and  density,  differ- 
ence between,  226 
supernumerary,   287 
Tenderness  to  pressure  in  pericemen- 
tal infection,  425 
Teratomata,  148 
Tetanus,   172 
Thrombi,    74 

agglutinative,   88 
annular,  88 
arterial,    88 
ball,   88 
calcified,   89 
canalized,  89 
capillary,  88 
cardiac,  88 

glutinative,  88 
hyaline,    88 
infective,   89 
in  peridental  membrane,  410 


Thrombi— Cont 'd. 

lymphatic,   88 

marantic,   88 

obliterative,  88 

organized,  89 

parietal,    88 

polypoid,   88 

portal,   88 

primary,  88 

propagated     secondary),  88 

proximal,  88 

red.    88 

saddle,   88 

stratified,   88 

types  of,  87 

valvular,    88 

venous,  88 

white,  88 

yellow,  88 
Thrombosis,   87 
Thrush.   571 

pathologic  anatomy  of,  572 
Ticks,  196 
Tinea,  circinata,  184 

favosa,   183 

sycosis,  184 

tonsorans,    184 

trichophytina,   183 

versicolor,    184 
Tissue  ehanges,  progressive,  111 
Tissues,   investing,  destruction   of,   by 
salivary  calculi  tobaeosis,  64 
Tomes,  fibers  of,  505 

granular    layer    of,    231 

zone    of    344 

zone  of,  possible  etiology  of,  346 
Tongue,  affections  of,  572 

leueoplakia  of,  573 

ulcers  of,  572 
Tooth    brush    friction    and    abrasion, 
356 

development,   first    evidence   of,   242 

follicle,    fibrous   envelope    of,    233 

impaction,  291 

incarceration,  291 

movement,  following  extraction,  379 

peg-shaped,  supernumerary,  287 

powders,   gritty,   and   abrasion,   356 

protrusion,  436,  433 

sensory  organ   of,  501 
Toxemia,  154 

Toxic  products  from  burned  tissue,  42 
Toxins,  153 

intracellular,   153 

soluble,  !'>■] 
Transparent  zone,  344,  510 
Transudation,  95 
Traumatisms,    39 


INDKX 


:,!i:; 


Trematodes,    L95,   196 
Treponema   pallidum,   L68 
Trichinosis,   204 

Trie! ephalus  dispar,  202 

Trichomycetes,   L80 
Trichophyton,    183 
Trypanosomes,    pathogenic,    186 
Trypanosomiasis,   186 
Tuberculosis,  164 

;iinl  mouth  infection,  •"(>! 
secondary,  167 
Tubular  calcification  in  abrasion,  358 
Tubuli,  dentinal,   228 
a  field  of.  220 
anastomosis  of,  230 
average  diameter  of,  348 
calcific  degeneration  of,  510 
curves  of,   231 

in  bicuspids  and  molars,   230 
in  incisal  region,  230 
in  relation  to  cusps,  231 
penetration  into  enamel,  232 
relative    diameters    of,    230 
Tumors,   113 
benign,  115 
classification  of,  116 
habit  of  growth  theory,  114 
inclusion  theory,  113 
irritation  theory,  113 
nervous   theory,   114 
parasitic  theory,  114 
predisposing   causes,    114 
primary,  115 
secondary,  115 
theories  of  origin,   113 
Typhoid  fever,  174 
Typhus   fever,   194 
Ty rosin,   524 

U 
Ulcer,  104 

follicular,   104 
fungous,  104 
gangrenous,  104 
indolent,  104 


i  leer   -Cont  'ii. 
of  tongue,  572 
peptic,  104 
phagedenic,  l('l 

rodent,    1  1 1' 

serpiginous,   104 

specific,  104 
Ulceration  form  of  infection  of  pulp, 

530 
Uric   acid  salts   in   Mood,   496 


Vaccination,  154 
Varicella,   191 
Variola,  194 

Verrucas,   136 
Vesical  calculi,   70 
Vincent's  angina,  179 

Viscosity  of  saliva,  316 
Vital   resistance,   214 

conditions  which  lower,  214 

lowered,   214 
Volkmann's  canals,   455 

W 

Wandering  cells,  99 
Warts,   136 
Wheals,  95 
"White"  clots,  75 
Wombstones,  132 
Worms,  round,  196 


Xanthoma,  128 
X-rays,  effects  of,  44 


Yeasts,  152 

Z 
Zone  of  Tomes,  344 


COLUMBIA   UNIVERSITY    LIBRARIES 

This  book  is  due  on  the  date  indicated  below,  or  at  the 
expiration  of  a  definite  period  after  the  date  of  borrowing,  as 
provided  by  the  library  rules  or  by  special  arrangement  with 
the  Librarian  in  charge. 

DATE   BORROWED 

DATE   DUE 

DATE   BORROWED 

DATE   DUE 

MAR    81& 

" 

'•J 

\<&% 

m 

jy(4 

C28 ( 546 ) M25 

RK301 


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